Forum: Niman III

DEMfromCT, how about a new Niman III thread?

Thanks pogge.

You got my attention. Wasn’t the Niman III thread going to happen when he made his latest announcement?

H5N1 stays on track

http://www.recombinomics.com/News/02090603/H5N1_Nigeria_Children.html

I have a perhaps stupid question for Dr. Niman…

Dr. Niman, in a commentary on January 12, 2006 you wrote: “The latest results indicate H5N1 continues to acquire mammalian polymorphisms via recombination, not random mutation, and these acquisitions are leading to more efficient transmission of H5N1 to humans.”

Here’s my perhaps stupid question:

Is it useful to look at which potential mammalian polymorphism recombinations we might see in future based on which lead to better outcomes for the wild birds? In other words, is the reason the PB2 polymorphism E627K was transported in migratory birds from Qinghai Lake because that change made H5N1 less lethal to hosts and therefore those birds were able to migrate while carrying the virus? Likewise, did the S227N change make the virus even less likely to cause die-offs that would prevent migration? Is the virus “intelligent” enough to keep aiming for recombinations that would ensure its dispersal more reliably, and should we be searching for possible recombinations that reduce the pathogenecity (sp?) to birds (and perhaps more transmissible to humans only secondarily?)

As a corrollary: will large die-offs of wild birds become a less and less reliable indicator of trouble as the more dangerous recombinations occur?

once the bird flu goes efficient H2H, will it still be called bird flu? Or something else?

kristy - I have been wondering if the media would come up with some other catchy name for this beast.

Once a virus becomes efficient at infecting humans, it becomes a human virus. The first human H2 (H2N2) started the 1957 pandemic and the first human H3 (H3N2) started the 1968 pandemic.

Hillbilly Bill – at 14:50 - I am wondering too.

I am coming across people who have “BIRD FLU” ingrained in their minds, so they think that its “only birds” that are at risk.

It wouldn’t make sense for the media, or even our government to continue calling it Bird Flu once it becomes effecient H2H.

Hillbilly Bill, I agree with you. I have also heard comments along the same line. As things have to start from some place maybe we should start here by refering to this pathogen by a some new standardize name. My suggestion would be Av/flu. Or something along these lines. So as not to allow people to combine a false image of security with thier proximity to birds.

at that point it’s panflu or pandemic flu.

“Pandemic H5N1” works for me…or pandemic influenza (the “flu” just is too familiar and already discounted by the public).

I hope Dr.Niman told “those who need to know” something that will make them be able to make better outcomes for us all…

My name suggestion: “Lung Eating Virus” (“Flesh Eating Bacteria” was such a sexy name, it got lots of press.)

Too long? What about “Lungrot”?

Captain Trips??????????????????

Not bad, April. But to legitimize it, it needs an acronym.

How about VSD? VIRAL SMURF DISEASE aka Viral Bluemonia

(smurfs are what ems call people with cyanosis)

A Family Cluster Now in Iraq? The following quote from today’s ABC News article Control of Bird Flu Difficult in Iraq would seem to be consistent with a family cluster, wouldn’t it?

Children suffering from bird flu-like symptoms are seen in a hospital in Sulaimaniyah

“On Tuesday, health officials in the southern city of Amarah said they were investigating the suspicious death of a 14-year-old pigeon seller who suffered bird flu-like symptoms. On Thursday, Amarah authorities said three of the dead boy’s cousins two brothers and their sister have been hospitalized with similar symptoms.”

Sure, the one boy played with pigeons, but so many family members, and the delayed onset of the flu conditions relative to the boy who had the pigeons.

PanFlu5.1 or PF51

But “only” upon “efficient” AND “sustained” H2H defined and agreed by WHO/CDC/BSIC at > 103 dispersed locations each w/ RTRT-PCR-confirmed cases > 10.

oh yes . . . and no birds vectored within 9.86 km of said locations.

Fair enough?

Or maybe not?

PF51 almost sounds like an airline “flight” number. Well, I guess, we are all waiting to be advised of the arrival time and the gate?

HN51 as homage to accurate and useful predictions? Hint - H does not = HA spike.

I like PanFlu, it has a nice sound to it and is quick to say which is necessary for reporters who have to say it over and over. I saw bottom scroll on CNN about avian flu this morning. Maybe some people are waking up.

Family cluster in southern Iraq

http://www.recombinomics.com/News/02090602/H5N1_Iraq_Cluster_South.html

and northern Iraq

http://www.recombinomics.com/News/02060601/H5N1_Iraq_Cluster_Growing.html

How about Mutated Avian Human Influenza (like Mahi Mahi fish)

In the US birds chickens are not a problem but cats are. How about cat rot?

Dr. Niman, I am hoping you might check this thread, read this, and respond—is there a possibility that the diagnosis of avian cholera that was originally given in Nigeria is what is happening here in the US with the Salt Lake avian cholera and the Arkansas avian cholera cases? Do you think it will be announced say in two weeks that it is actually H5N1?

Mother of Five: Based on the postings last night and today I think you and I seem to be among the very few who appear concerned about the American “bird cholera” cases…

Again, this is how it began in Nigeria. Are the scientists absolutely sure this is not H5N1? Any scientific opinons out there in FluWikieland?

docdoc – at 10:05 - I like MAHI !! The “MAHI” virus of 2006.

Dr. Niman… I have been keeping up with your recombinomics comentaries & find that you do seem to have a jump on the rest of the experts… I would like to ask you a question… In your expert opinion what is the next predictable recombination & what effects will we see from it in the virus???

I totaly agree with wild bill, Likewise for what it’s worth i would also like to know?

Even a hint at when you will reveal your latest would be appreciated.

I also agree.

Anastasia—thanks for the back up. I am still uncomfortable posting too much. I am not a scientist. But, I have been following this site and the subject of bird flu since August and have learned so much and am PAYING ATTENTION—unlike so many of my friends and associates. I am so worried about it being here already and that they’ll only admit it when the media gets word that its infected someone already. I don’t want my family to be patient “0″

Mother of five, Please don’t feel uncomfortible about posting too much. Speaking only for myself, I think that true interest in any subject is enough to be qualified to form an opinion on a issue. Granted that you take the time and effort to learn what you can about that issue. Which you seem to have. What you have to say is welcome.

niman,

You say, “Confirmatory lab tests are becoming increasingly suspect. Of the 21 H5N1 positives in Turkey, only 12 have been confirmed. The negative data on the other nine raises question about the collection, storage, and shipment of samples. The inability to confirm H5N1 positives by outside agencies is rare, but reliance on clinical presentation is becoming increasingly important. The index case in Iraq was initially said to be negative, as were the four siblings in Turkey.”

“Although H5N1 has become increasingly prevalent since the explosion of infections in Asia in 2004, the testing appears to be getting increasingly unreliable. This unreliability is most obvious in clusters.”

You go on to mention several political aspects of unreliable testing, but I’m still not sure why lab testing should be increasingly unreliable.

Test technology notwithstanding, the WHO test regime is clearly unfit to purpose. Missed opportunities to test, false negatives, long distances and times from field to lab, contamination of samples, tardy announcements…perhaps not all it might be. Can you suggest any technical or procedural remedies these deficiencies? Is the test regime bound by money? What good might come of using some of the H5N1 quick test kits? I can’t conceive how anything so patently crucial and inadequate can’t be dramatically improved.

The next recombination will be announced shortly. Here’s a clue

http://www.recombinomics.com/News/02100602/H5N1_Lagos_EAF.html

looking pretty ominous here

When you say “shortly” do you mean shortly as in later today? Or shortly in a week from now?

Based on the events of the last few days, I’d say we’re all pretty anxious to hear your announcement.

Still getting my “ducks in a row” so to spreak.

Gotcha.

Actually, looking at the new map you had in your commentary regarding the East Atlantic Flyway, I think I can already piece together where you’re going with this.

Looking forward to your commentary when you’re ready.

quack quack, argghhh, thump…..(taps playing da da da…….da…da… DA..da…da…DA..DA..DA…DAAAAAAA…da…da…da…………..da…da.da

As far as monitoring H5N1 in the US goes, there results from Canada were pretty straightword. As part of an August banding program, they swabbed wild ducks. A few months ago they announced H5 was widespread throughout southern Canada. Although it was several different low path serotypes (H5N1, H5N2, H5N3, H5N9),

http://www.recombinomics.com/News/11190504/H5_LPAI_Quebec_British_Columbia.html

http://www.recombinomics.com/News/11190505/H5_Canada_Test_Concerns.html

there were some positives on a farm in British Columbia that led to a significant amount of culling and an OIE report

http://www.oie.int/eng/info/hebdo/AIS_42.HTM#Sec11

The H5N2 was similar to H5N2 in California.

There is little doubt that the H5 in southern Canada in August entered the US. H5 is now a reportable disease, even if it is low path. The US has not made any reports since the Canadian announcement. The US surveillence has little credibility.

Lame ducks…

So you’re saying that H5N1 is already in North America?

No Kristy, all probability though, the right keys are in place to bring it here being thatt the eastern flyway overlaps with western africa . 3–4 months if not sooner, unless ofcourse it goes sustained H2H, then who knows.

Isn’t he also saying that H5N1 will could become a flu within swine and birds, transported to North America by migratory birds, and since swine are so much like humans, this is worrisome and a probable way in which this flu could become a H2H disease? Atleast that’s how I’m reading into it all. I just keep noticing his references to mammals.

Thank you Eric.

It’s been a long week for me, and my brain is on sleep mode today, so thanks for breaking it down for me.

OK … I may be totally wrong on this and I am more interested in learnin the facts that being right so go ahead and correct me.

First off, H5N1 is being transferred to humans by birds by contact with sick birds. Does this include EATING infected birds? I mean is this a common means of transmission?

Second, is if being said that H5N1 will then combine with swines and create a bird to pig infection route which would mean that pigs could then also be a transmission point for H5N1?

If the two above are true does that mean that both poultry and pork supplies are going to be in danger … meaning nonedible?

Pigs getting sick in the middle east isn’t a problem economically speaking because practicing/Orthodox Muslims don’t include pork in their diet.

Pigs getting sick in other places to the point that they can transmit the H5N1 will be a much bigger deal as pork IS a larger source of protein.

Also, if all the above are true then culling pigs is going to be a much bigger and messier deal that culling poultry in my opinion. I know when my granddaddy killed hogs it was certainly a bigger deal than when we would cull the flock of chickens.

Am I in left field with this? And I’m certainly not overlooking the pig to human infection factor, just trying to get the basics down before I head off onto that particular road.

sorry for the ripped up grammar in my previous post … trying to type with a two year old in your lap is a losing proposition

Kathy, I think his references to polymorphisms with swine indicate that he’s concerned about the virus taking on the ability to easily transmit to mammals, but to also be able to be transported via the migratory birds. It seems to me that it is very important for the virus to remain a disease of migratory birds if it is to eventually become a human flu pandemic. This is all with the assumption, of course, that it doesn’t recombine within Nigeria and become a human to human problem there. With all 3 migratory routes overlapping in Lagos, creating a see of genetic variation for the virus, that seems to be of great possibility.

I wish I would reread things before I post them. For example, I meant “sea,” not “see.” I too have a couple little distractions running around the living room right now. lol

OK, I think I get it and thanks for helping me unscramble it.

The recombination part is still over my head, but I’m learning. Mutation I can get my head around, recombination is a new concept for me. I think that is a lot of people’s problem. The H5N1 would seem to be less likely to mutate to a H2H version and the concept of mutation may be all they know. However by recombination it is much more like to go H2H, but most folks don’t know about the idea of recombination. Its a foreign concept.

Dr. Niman still hasn’t addressed Mother of Five’s question regarding the 30,000 dead birds at the Great Salt Lake and the 1,500 in Arkansas who have all supposedly died of avian cholera. Is it possible it is someting other than cholera? Could something have come down from Canada? It would be appreciated if we could get a scientific take on it…

Does anyone know the current status of H7N7 in Western Europe and/or U.S? Reading over a report on the outbreak in Netherlands in 2003, was struck by both the similarities in genetic characteristics to H5N1 (and clinical symptoms in the one poor man who died) and the (to researchers) surprising level of H2H transmissibility of the virus. When it hit in 2003, most of the human cases were relatively mild, but the one fatal case acted an awful lot like H5N1. If current H5N1 down in Lagos moves north and meets with this H7N7, seems like it would not be a good thing. However, I have no idea if it’s still around in bird populations in Netherlands, Brussels, and Germany or not. There were also some H7 outbreaks in US around same period, I believe, but I have no idea if was same strain.

The only way to know about bird die offs in the US is to test. The groups testing believe dead birds don’t fly and H5N1 isn’t transmitted or transported by migratory birds.

There are many ways to get false negatives and since the US hasn’t reported the H5 from Canada, the clearly are not trying or reporting. Lack of reports of H5N1 in the US doesn’t mean H5N1 isn’t already here, but reinforcements are clearly on the way and H5N1 will have gone global in the next 12 months (possibly by fall of this year).

Dr. Niman… Thank you for your reply… I am wondering if H5N1 will pick up a mutation from recombination with H1N1 or Reasortant H3N2 possibly in swine in the US or Europe???

Dr. Niman: Thanks for responding to our questions. Very appreciated.

PS. I asked my veterinarian her thoughts about H5N1 being in the US. She gave me a very guarded look and said that the “powers that be” would try to keep it hidden as long as possible…

 …”the American “bird cholera” cases”… have me concerned/discouraged too.

worst case – at 16:06 Just open up a word processor. Type your comment there, work it out and then copy and past it.

WildBill, Very good question. Look for an answer next week.

Bravo Bill! A piece of the puzzle.

Cheerio!

Bill and Doc…

From another board, “Once the current Nigerian Bird Flu mixes with a possible Swine Flu outbreak currently in northern Uganda , watch out.”

Lovely, aye?

I like the name “CAptain Trips”…but I suspect that this one will be known as Bird Flu no matter what. I worry about the swans dying in England. But the Brits say it isn’t bird flu…

There is another influenza, canine influenza, that has been seen in the last 2 yrs in the US, which apparently originated in FL and is thought to have jumped from horses to dogs, crossing the species barrier. My understanding (and I am not a scientist!) is that it is also an avian-type influenza. Dr. Cynda Crawford at the University of FL has spearheaded research on this canine influenza, which has caused the death of numerous racing greyhounds across the US, and also has been seen in numerous animal shelters, particularly in S. FL. I have no idea what the H or N of that influenza is, although perhaps one could find some reference to it by doing research. I can tell you it is a very dangerous and deadly disease in dogs. That influenza is not transmissible to humans in its present form and one would hope it stays that way. Mary.

Ok, so the swine in Europe have in common a varaint that was found in a child in 1999 - and the same varient is in the birds from China that went to Turkey So whats going to happen when these birds fly north to Europe and meet up with the swine? Seems like they are already kissin cousins - are we gonna have some intermarring?

Geez I dont even know what Im reading half the time

From CIDRAP:

http://tinyurl.com/dfdq8 [snip] If H5N1 continues to circulate widely among poultry, the potential for emergence of a pandemic strain remains high. For example, H5N1 viruses have been found in pigs in southern China, and human H3N2 influenza viruses are endemic in pigs in that area. H5N1 has recently been reported in pigs in Indonesia as well (see References: Cyranoski 2005). Thus, the conditions exist for exchange of genetic material between the different viruses in the pig host (see References: Li 2004; WHO: Avian influenza: update: implications of H5N1 infections in pigs in China). Some scientists believe that reassortment between an avian and a human strain could occur in the human population without an intermediary host; if this proves true, as more humans become exposed and infected, the potential for reassortment with a human strain may also increase. [snip] It seems it does not have to be Europe or the Americas….but we have looked at this before on these threads..what is new?

Dr. Niman, does your coming announcement have anything to do with this?

http://www.haloscan.com/comments/revere/113219520791370390/ ….”Why does both the Chinese and US CDC refuse to release information regarding specific strains of the bird flu virus, is it because it would be immediately noted by Henry Niman that the strain was genetically engineered?….

Just guessing in a paranoid kinda way…

Actually, I just want you to discount this as paranoid rantings maybe… that would be nice

Just on the news in Phoenix, hospital overflowing with a respiratory flu. Beds lining the hallways. Sounds different than the flu earlier this season. Sounds a bit like what was happening in 1915–16.

I don’t buy it. China is NOT behind this in a preplanned way.

A virus makes a terrible weapon of choice. They do what they want and don’t care if your country is the “Mother Land” and your chairman the father who help create it. It will still infect their country and its leadership. It will then move on and on.

(But only as a mental exercise…) On the other hand, it could be war. They act like it when they brag to their population that they will beat the BF by their technology, that they have a huge accumulation of sequences that they will not share, that they can rush large amounts of vaccine quickly to those in need. They could even loose half (or more) of their population and be better off. Would they have a dream of emerging from a BF pandemic as the only world power left?

I still don’t buy it.

Thank you, Dr. Niman, for your comments. I appreciate it. I finally bit the bullet and took my chickens to a nearby farm. However, as we went outside this afternoon, I discovered one of my chickens was already dead in the pen. It wasn’t dead yesterday afternoon. I am the one who posted a while back about my hens dying such terrible deaths and the vet thinking it was no big deal. They sent the last one (in September) to a lab and called me eight weeks later to say it had an infection in the blood. “That’ll be $100″ I asked if it were contagious to other birds, children, other animals, and what the infection was called, etc. The vet says “Well, I think I better check back with the lab and find out a few more things. We’ll get back with you.” I haven’t heard from them since. I feel very challenged to take this most recent hen in for testing. I’ll gingerly throw out the suggestion that I would like some feedback????? I don’t know what to think anymore? I am so tired of everyone, including my husband, thinking I am silly. I hate that word! I am so annoyed with him right now because he was happy to be getting rid of my birds. I love those birds! Being a city-slicker growing up, I thoroughly enjoyed playing “Green Acres!” I enjoyed the independence of collecting eggs and not having to purchase them at the store. Anyway, I moan, I apologize.

Dude, thanks for replying. I don’t want to buy it either. I’m just putting together some things… Here, e.g. is the map for the bird flu from May…

http://www.recombinomics.com/H5N1_Map_2005_QinghaiLAni.html

Here, e.g. is the map of China showing where Xian, Shaanxi, China is located.

Xian is the location of “Xian Jiatong University is a known center for Chinese army biological and chemical warfare research.” from this link:

http://www.newsmax.com/archives/articles/2001/12/5/231538.shtml

As you say Dude… just a mental exercise. There are conspiracies everywhere if we look hard enough I guess. I’d just like to be told I’m insane and leave it at that…

oopsss… forgot to put the link in for the map location of Xian… sorry…

http://www.travelchinaguide.com/map/index.htm

oopsss… forgot to put the link in for the map location of Xian… sorry…

http://www.travelchinaguide.com/map/index.htm

Sorry to hear about your chickens, mother of five. But on the bright side, I’m sure it will give you more peace of mind, with what’s going on.

As far as your 2 dead chickens, why don’t you try to contact the vet about the first chicken that died and see if he can put a name on what that chicken had? He may have the information by now.

If you plan to take this second chicken in for testing, I would try a different vet/lab, and make it clear up front that the reason you’re paying for the test is to actually receive some information out of it. Maybe you should ask for a refund in the first case, since you didn’t get what you’d paid for?

Once again, I’m so sorry you’ve lost your poor birds. One day, hopefully, when all this has passed us by, you’ll be able to start up with a new bunch of healthy chickens.

And this link confuses me… isn’t this the HPAI ? And there’s a vaccine for birds?:

link

Oh well… enough of this nonsense I’ve gotten myself looking at… I obviously need sleep…

Dr. Niman,

I read somewhere on the web today that certain scientists are downplaying the risks of Human-to-Human H5N1 with the rationale being “H5N1 has been around for 8 years and hasn’t gone human-to-human yet, therefore it is unlikely that it ever will. Past Pandemics (such as 1918) tranformed over a much shorter time period from an avian to human virus.” Should we take any solace in the lack of evidence of easy human-to-human transmission 8 years after H5N1 was first found to infect humans?

Thanks, DSR

Announcement will be on recombination

http://www.recombinomics.com/News/10220501/H5N1_H9N2_Recombination.html

and acquistion of polymorphsims

http://www.recombinomics.com/News/01190601/H5N1_Turkey_S227N_E627K.html

No genetic engineering required.

mother of five, Please keep posting, I’m following your posts and any responses you get. You bring up some important points! - mother of six

I think I understand Dr. Niman. Thank you.

Not meaning to ignore you mother of five. I would feel the same way you do if I had to give up my chickens. I don’t have any but my neighbour does. There’s something wonderful about chickens in the back yard. I’d report your dead ones to somebody though… Sea Urchin’s idea about the vet sounds like a great idea. Hang in there.

I think I understand Dr. Niman. Thank you.

Not meaning to ignore you mother of five. I would feel the same way you do if I had to give up my chickens. I don’t have any but my neighbour does. There’s something wonderful about chickens in the back yard. I’d report your dead ones to somebody though… Sea Urchin’s idea about the vet sounds like a great idea. Hang in there.

Thanks for your comments and support, Sea Urchin and Laura in PA. It’s funny the things we find ourselves becoming attached to :) We also have a whippet, which is the medium-sized greyhound breed. I am worried now about some new canine influenza they say is affecting the track greyhounds. Someone posted here, I believe, about it. I don’t know if it has anything to do with avian influenza—there was also an article about the dogs in Turkey dying in large numbers and if I remember correctly they traced it to the dog food. So what, did they make the dog food with infected poultry? I have no idea. But we are not getting rid of our dog! She is a treasure and I draw the line. We will house train her to go in the house if we have to keep her inside (that won’t be hard :) ) I am so glad for fluwikie. It’s nice to know that we’re not alone in our concerns. And, Dr. Niman, I really want to express my pleasure to read your posts. Not that the news is always pleasureable, but it helps me feel that if this becomes an issue TODAY—HERE—then we at fluwikie will be the first to know and it may give us a minute edge on finishing up preps. Thanks again.

mother of five, i heard about a pet food recall here in the US and a lot of dogs died. See this link http://www.msnbc.msn.com/id/10771943/ perhaps Diamond (I think that 2 other companies were involved, also). very sad.

correction: perhaps diamond shipped internationally. I’d better get some sleep!

I’ll check it out, Laura in PA, thanks.

BTW, Dr. Niman, I was picturing you as sort of a Jimmy Stewart looking kinda guy? Is it just getting too late in the morning—early in the morning??:)) I think I’ll check back here sometime after I get a little sleep!

DSR, Solice not advised. The story is in the sequence

http://www.recombinomics.com/News/02110601/H5N1_S227N_Transport.html

Diamond dog foods were the brand recalled because of aflatoxin, and they did ship product internationally, and some dogs have died overseas as a result. No need to give up your dog; he sounds like a sweetie! Canine influenza is real, but it is being seen in kennel situations where dogs are in close contact. I would be hesitant to board my dog if there are reports of canine influenza in your area.

Although H3N8 can be common in kennels, it has spread beyond kennels

http://www.recombinomics.com/News/09270502/H3N8_Companion_Dogs.html

Dr. Niman, thank you for the reference re canine influenza. I have particular interest in that subject because I do dog rescue, and we unfortunately had influenza go through our kennels 2 yrs ago, brought in with dogs transferred from a shelter in south FL. I do have a question (but don’t know if anybody has an answer.) If a dog has contracted H3N8 and survived, would that animal then have immunity to the virus? How long would that immunity last? Same question regarding H5N1 - the people who have survived it, will they now have immunity to the virus should they be exposed again?? How long would immunity, if there is any, be expected to last??

Dr. Niman,

Thank you for your earlier reply.

Would the aquisition of PB2 E627K and HA S227N by H5N1 mitigate its virulence as it increases its human-to-human transmissibility? i.e. If it is more efficient in binding to throat and nose cells and less efficient at binding to the lower respiratory tract cells will it be less likely to cause the ARDS/severe viral pneumonia type sequelae that seem to cause so many deaths?

DSR

There are a good number of fatal cases in Iraq and Turkey. I think the milder cases are related to dose, not presence or absence of S227N.

Influenza changes regulalry to evade the immune system, which is why people get the flu again and again.

S227N makes the transmission more efficient, but not necessarily less lethal

http://www.recombinomics.com/News/02110604/H5N1_Iraq_Cluster_Amara.html

Mother of Five: I hope that $100 went to perform a necropsy (animal autopsy) by a board certified veterinary pathologist or avian practitioner. In either case, there should be a pathology report complete with gross and histological analyses, with cause of death and in some cases a small discussion of the disease in question. Ask your vet. for a copy of the necropsy report. If that was not done, and you have another chicken die, you may want to consider taking it to your nearest vet. school to have the necropsy done. You will then be assured that a board certified pathologist looked at the animal and you will have the true answer. For best results, keep the carcass refrigerated and get it to the vet. school or lab ASAP. It is not stange to love other living things! Even Dr. Niman felt compelled to share information on canine influenza. Most of us love the natural world around us and are devastated by the events we see unfolding. Thanks, Dr. Niman for giving us the heads up!

mother of five – at 01:44, “BTW, Dr. Niman, I was picturing you as sort of a Jimmy Stewart looking kinda guy?”

Our beloved collegue: http://peeringintodarkness.com/radio/?p=6

Cheerio! 007

007 in the USA - thank you for a great link.

Why didn’t we know about this radio interview before????

I think he is more Richard Dryfuss/Steven Speilberg with a midwestern accent…

He is my hero.

Quite a few interviews are at

http://www.recombinomics.com/in_the_news.html

but I haven’t linked the more recent ones.

niman: “I think the milder cases are related to dose, not presence or absence of S227N.”

By “dose”, I take it you are talking about viral load?

Would a smaller load mean a milder case of flu? Would that ilder case then give immunity to a more lethal load of the irus?

ilder should be milder and irus virus - sorry out of town at a convention and typing on the hotel computer. Keyboard is very stiff.

He wouldn’t fo it but I will here is a picture of Henry Niman http://tinyurl.com/9mnmb

Dem please to tell us, when that what Niman states as facts differs from the “mainstream” views or is not yet commonly accepted…

That was supposed to be “do” not “fo.” Fingers sometimes move to fast. Its a pretty good story too that will explain what he is doing.

gs,

Niman is ‘way out of the mainstream and until he’s willing to show us some of the science behind his proclamations, he’s just a showboater.

Niman is way out in front and he seems to be right. All the others are “cya” types. The V2 bomb “screamed and cut out” just before exploding. We dont need to be blown up to know what the evidence is saying.

gs, many virologists see recombination as a minor addition to viral evolution, along with reassortment and random point mutation. That alone makes Dr. Niman neither wrong nor right; it’s simply a controversial point.

The data on clusters isn’t completely accepted either (in terms of what it means)… yet.

Eric,

Where’s your evidence? All you do is make pronoucements, never with any links to supporting data. Strangely, Henry has no data, either. The consensus science doesn’t agree with Henry and he can’t show us any reasons why it should. That’s not even good rhetoric, it certainly isn’t an argument.

See this from the Bulletin of the Atomic Scientist.

…

…

And that’s the key. Many internet rumors have proved false, including those published on Recombinomics. So, take what you read with a grain of salt and do your due diligence.

Finding proof is always hind-sight. Niman is showing were it is going. The proof will follow. We have to prepare as if Niman is going to be right. It will be way , way too late to prepare after “proof” is revealed. Sustained H2H is a forgone conclusion, its stil a matter of when and all of the pieces of the puzzle are falling into place. We have mechanism, transportation routes, natural human factors, historical precedent, greed, etc. Proof is all around us, yet some of us are sort of slow on the uptake.

Oh, I’m all for prep, Eric. I did sort of help start this wiki, you know. ;-)

I just don’t put Henry on a pedestal. I never asked him if he minds if other people do, actually. In any case, reminding folks of when niman is correct without reminding folks of when he’s wrong seems like a disservice, that’s all. The complete picture is the more accurate one.

Why not take that view about everyone? Well, we should, but there aren’t many scientists who have become aggressively known like Henry Niman. After all, how many people have a thread named after them? ;-)

One simple fact. 12 cases of H5N1 form Turkey were confirmed by Mill Hill and reported by the WHO on January 20 2006. Here’s the link. It is now February 11 2006. 3 weeks have passed and the WHO has not provided symptom onset dates for these cases or the relationships between the patients. There are only two explanations for this.

1. Gross incompetence

2. Cover up of large clusters

I go with Dr. Niman on this and choose number 2. Time will tell, but time is running out.

What Dem said a few posts up: never ascribe to malice that which can be attributed to simple incompetence. That and the fact WHO probably doesn’t have enough people on the ground.

A third explanation, that of careful detective work that takes longer than three weeks, also exists. You have biased the selection of choices to

1. I’m right
2. I’m right

wheras you forget

1. I’m wrong
2. WHO is right

As you say, time will tell.

PS For those new to Flu Wiki, Monotreme and I often debate this, with great respect on both sides. He might in the end be right, though it cannot be determined right now.

Melanie: It is inconceivable to me that no-one at the WHO thought to write down symptom onset dates and the relationships between the patients. They were on the ground in January, in Van. Surely they could afford a piece of paper and a pencil. But, I guess we all have to interpret their actions in our own way as they answer to no-one.

I agree with DemFromCT at 19:25

but not at 19:22 ;-)

In any case, the arguments have been presented. People can make up their own minds as to the most believable alternative.

Actually, Monotreme, they answer to all the member governments, which is both their strength and their weakness. If the members demanded this stuff, they’d get it (which doesn’t mean they’d tell us about it.) The member nations are all suspicious of any UN type program and chronically underfund them. They are chronically short of personnel for a global pandemic as well.

I know…you and melanie are right about proof. I also know the media and those who control it. What goes on behind the scenes is what frightens me. The silence is deafening (spelling?). I stay a faithfull follower of fluwikie

Heh. Data is persuasive. The lack of data starts arguments. ;-)

Melanie: “If the members demanded this stuff, they’d get it”

Agree completely. Hence my many posts on this subject. I’m desperately hoping some government type reads something here and starts demanding answers of the WHO. Its a long shot, but I feel I have to try.

WHO knew EXACTLY what they were doing when they left out disease onset dates (most important piece of info) and relationships (second most important piece of info) for the Turkey clusters.

Arguments of overwork, or incompetence are not reality based. In fact Klaus Stohr was quoted in the media with regard to two large family custers BEFORE the WHO updates came out.

None of this is at issue and the interpretation is VERY easy.

Alternate explanations are utter nonsense.

Turkey was a VERY big deal and was a VERY big cover-up in plain view for all to see (all one had to do was pay attention).

Dr. Niman: First dibs on a signed copy of your coming investigative history of this debacle. (Assuming we both survive. Damn! There is always that “qualifier’ intruding into these delightful threads).

Here’s what the WHO teams say:

Maria Cheng, a spokeswoman for the World Health Organization, said her agency suspected that there might be human cases of A(H5N1) flu in Africa, but had no way to confirm that yet.

“We’re getting a team ready to go,” she said, “but we’re waiting to get the invitation from Nigeria.”

I agree with Dr Niman. The proof is out there. One only has to decifer. I would rather (be prepared) and in the “I told you so” camp and be wrong than in the (I’m not prepared) “There is no need for alarm yet” camp and be wrong.

While this is on the subject of past turkey cases and “cover-ups”….has anyone yet heard post mortem results on the 4 year old girl who died there? The one the doctors were absolutely positive did not die from BF as they did a thorough investigation and found she had no contact with birds, no contact with preparing chicken or had eaten chicken. But her symptoms were suspect enough that they decided a post mortem check had to be done. I posted this question about a month ago, suspecting a cover-up as no info had come out, and no one here had any updated info at that time. How ‘bout now? or do they still think this is worthy of continued cover up even though we all know there has been other cases of H-H since then?

Turkey is clearly NOT looking for cases. The youngest of the four siblings (the chicken head kicker), is STILL an unconfirmed case. There is no doubt that he was H5N1 infected, yet the number of confirmed cases is 21 and counting down to 12. Hatice Ozcan was admitted with two siblings who were H5N1 positive and placed in the ICU. The is little doubt that she had symptoms and was H5N1 infected, but she also remains a negative.

Data on clusters are VERY revealing and Turkey has NO interest in finding new cases. The suspect cases get placed in isolation and are treated with Tamiflu. No H5N1 positive lab test required.

sorry that i just can’t let this go, but this case of the 4 yr old really intriges me. reason being, she was not involved with a family cluster. had no siblings or other family members who were ill. No known exposure to infected people. Her obvious H-H did not include or rely on close family contact, as the other cases have. She just came down with it “out of the blue” from no apparent source. H-H from brief exposure from infected others walking the streets? Any input from anybody’s thoughts on this? Thanks

I am not a medical expert or a scientist, but there are some things here that just don’t make sense.

I don’t see how WHO could not have data (disease onset, etc.) on the cases in Turkey. The admitting hospitals would have info, documentation is part of the process of admission and continues through the course of treatment. I don’t understand why they would not be collecting data on and testing new suspected cases- epidemiology is studying the progression of a disease in individuals and in an affected population, is it not? I don’t see how collecting that data could be reasonably left out of the equation regardless of man-power. Is it true that no one is testing suspected cases in Turkey anymore? If true, that is very shocking to me considering how much is riding on how this virus may change. Without that information there is no proper study.

So, the information must have been collected. It doesn’t make sense that epidemiologists would not continue to track new cases- so the information must still be coming in.

The question then is, where is it and why is it not being released? What is the usual time frame for data to be released? Is this an unusual time lag?

Dr. Niman: Any more available info on the Indian sailor who died in Lithuania?

Remember that Turkey is not Europe or North America. Their surveillance systems are not ours and not everyone can get to a hospital. Most of these cases are anecdotal press reports, and we know already that the press isn’t doing a very good job.

And as Dem said earlier, serum titers take a couple of weeks to be processed. You can’t make the tests worker faster than they can work.

Forgive me if this sounds ignorant or stupid, but I do wonder what benefit these countries have from covering up cases?

Melanie at 21:22: Was that in response to my question regarding the Indian sailor? I ask because on the News Reports 2/11 thread someone posted a couple articles that said the sailor tested negative. But, has it been long enough to have an accurate test run? Just curious…

Anastasia,

Serum titers are the most accurate tests and they take a couple of weeks for results. I don’t remember the date of the Indian sailor story any more. It’s all become a flu blur in my poor brain.

No economic fallout that way, Kristy;

other governments may enact import bans of their products, travel warnings may go out to business and vacationing travellers, keeping their money away.

If a nation is found to have high-path H5N1 there are consequences they don’t want to have if they can avoid, or at least, postpone them.

What would happen to the US stock market, poultry-related food industries, conventions, international students and our tourist industry if H5N1 was killing hundreds of thousands of birds in our country, and kids and adults were getting sick and dying? (We may get to live through the answer, given enough time.)

In the past, some governments are said to have told doctors what they can and can’t write down as a diagnosis. (Radiation from Chernobyl, HIV, SARS, whatever.)

Pretty easy with H5N1 it sounds like, to take the wrong test at the wrong time and get a result that will keep your government from being displeased with you.

Thank you fullmoon. I agree that governments are covering it up, I just needed a good concrete answer to give my friends/family during conversations regarding this issue.

I repeat what I said earlier: the science (and data) in this area have enough unknowns that you don’t have to assume malice on the part of WHO or governments. The folks in the science community are scratching their heads about much of this. H5N1 appears to be a genuinely novel virus and making predictions about it would be scientifically irresponsible.

I think to NOT make predictions on it would be devestating.

hey, why can’t we have several Nimans ? Why is there only one ? The subject is certainly important enough that we could afford some more qualified people working independently on the issue. On our, -the people’s- behalf and not for governments or government-organizations. The science/topic and Niman’s equipment doesn’t seem so advanced, that noone else could do it. I don’t feel comfortable with just one opinion only, which isn’t being challenged by others doing the same scientific/journalistic/prediction/prophetical work.

gs: There are lots of people working on this issue. Some of them may even post here. They are not as vocal as Dr. Niman when using their real names, for various reasons. The most vocal expert is Michael Osterholm. Although he is more diplomatic and more cautious in his statements than Dr. Niman, he clearly thinks its important to prepare very seriously, very soon. So does Dr. Nabarro. So does DemFromCT. So does Melanie. So does Revere. So does anon_22. So do I. Although we may disagree on some issues, the WHO, recombination, the final fatality rate etc. there is surprising unanimity on what the pragmatic steps that should be taken. Don’t let the debates on technical or political issues obscure this fact.

Melanie – at 19:20

“…and the fact WHO probably doesn’t have enough people on the ground.”

Melanie, who should be held accountable if WHO (still) doesn’t have enough people on the ground? Should that possibility be tolerable, or should it have been recognized by the WHO executive months ago, and should that executive have then taken steps to remedy its deficiency? When does underfunding and ineptitude wear thin as an excuse for major shortcomings? To what extent are those shortcomings due to poor management?

I’m not saying the panflu picture is entirely bleak, but insofar as what WHO’s doing in the panflu arena isn’t cutting the mustard, shouldn’t personnel / organizational changes be made, or at least rung up for public discussion and debate? Hundreds, if not thousands of well-qualified people are available for restructuring if need be, and we may not have many more Turkeys to get WHO right.

You repeatedly state your aversion to politics in this forum, but I’m sure you must know that your Chewbacca Defense of The WHO is highly political. Why? Several reasons, but the notion that the WHO pandemic influenza program might be underfunded after several years of constitution reflects poorly on its major constituents. It’s almost universally known and accepted that the world is woefully unprepared. The WHO has accepted responsibility for organizing and managing the rapid containment force, yet in that very same draft protocol of acceptance, WHO confessed it had little present capability and wouldn’t have sufficient for six months or more if then. Regarding other more immediate responsibilities for which they might be underfunded or understaffed, they have little to say. Where’s their data? Where’s their candor? Where’s their accessibility? If making predictions about a genuinely novel virus would be scientifically irresponsible, issuing urgent alarms while tightholing pertinent information is socially irresponsible.

none of these people you mention gave probability estimates ! Except yourself.Are you a dr. too ? Apparantly noone except Niman predicted the Turkey mutations, I was told. Others are more careful with predictions and/or don’t post to forums. Osterholm,Nabarro are government,UNO employees they must serve the interests of their organization. Melanie is “risk-communicator” but apparantly considers probability estimates not a suitable form of risk communication, which makes me suspicious ! Dem is too careful (“we don’t know”), anon_22 too pessimistic (I think)and dislikes probability-discussion. Revere uses puns and details which are too tedious for me also strange logic sometimes and no predictions, of course. OK, I still appreciate them all. Can’t mention all their good points.

dubina: why do we have to rely on WHO alone ? If you just add more employees to WHO, they must all obey the WHO-directives. Let’s make a new,smaller organization instead so to have a second opinion.

Hi, you remember that the Turkish government has taken over the right to control all information about BF coming out of their country. They were saying at that time how mad they were that none of the other countries in the area were reporting their BF cases when the Turkish government was sure other countries had cases. So they got ticked off and decided that they would not be the only country in the area to suffer by being open. So it all got very quiet. It sounds like dealing with children in a playground with no adults. No mature judgment, resentment and petulance by the leaders in Turkey. The tragedy is that their actions constitute crimes against humanity if there are any cover-ups going on. I hope they remember that the whole world is watching. That goes for China and every country of the world. We will remember.

What do you think the US will do when we get the first case of BF in birds? Do you think the media will get hold of it? or be allowed to run it? And, if it does get out, do you think it will be downplayed? I do. I think they’ll do just like the other countries and try to keep it quiet—not so much because of international relations, but simply because of our own relations/economy. I’ll bet we don’t know that it’s here until we get our first human case of BF, and then we may not even know about it until there are several and they CAN’T keep it under wraps any longer. The world will be at pandemic level 6 for a short period of time before the world acknowledges that there really is a pandemic happening. That’s why so many here at fluwikie keep asking questions and find it difficult to tear outselves away—because we are hoping to be on top of it before it’s too late. I find I don’t even watch the news on television anymore—old hat. I wish I could come up with something clever to end with, like 007 :) I find after being away for just a day that things have passed me by and I have to play catch-up here at the wiki. “Boy, I’m out of it for a while and suddenly everyone gets delusions of grandeur” Name that movie? I think someone today posted something with a line from “Jurassic Park?” something something “bf kills man!” It was pretty good!

The large clusters in Turkey are well documented in media reports and they involve confirmed H5N1 positive cases as well as deaths

http://www.recombinomics.com/News/01220601/H5N1_Kocyigit_Ozcan_Timeline.html

These data are definitely glaringly absent in the WHO reports and WHO specifically said they were investigating these cases very carefully. They include all four confirmed fatalites. Comments that these are anecdotal press reports are nonsense. I didn’t read the remainder of such posts because they are annoying, at best.

Turkey is still reporting new outbreaks in in poultry. Iraq is still reporting outbreaks in people.

Just lookm at a map. The map says much more than anecdotal media reports.

http://www.recombinomics.com/H5N1_Map_2006_AfricaF.html

Map updated with new suspect fatal cluster in Iraq

http://www.recombinomics.com/H5N1_Map_2006_AfricaF.html

>Where’s their data? Where’s their candor? Where’s their accessibility? If making predictions about a genuinely novel virus would be scientifically irresponsible, issuing urgent alarms while tightholing pertinent information is socially irresponsible<

Well said Dubina

Solitaire

gs, I’m curious. Why haven’t you ever asked Dr. Niman for his probability percentages? I’ll bet he’s got some good ones. ;-)

dejure, I asked him in PM at curevent. Also several threads indirectly, nothing at recombinatorics either, nor in his posts - I searched for keywords. So I conclude he doesn’t want to give numbers. I estimated his estimate for a pandemic this year at 30% some time ago, AFAIR. Giving numbers for probability estimates is just not being stylish, I guess. Sigh.

dubina,

Chewbacca defense? That’s stretching things. The member states of WHO are ultimately responsible for its performance. The Director General is subject to them. If he doesn’t have the money and the personnel he can scream and yell all he wants but if the member states won’t give him the resources, the fault accrues to them.

gs – at 01:31

OK, I still appreciate them all. Can’t mention all their good points.

That’s because they’re way too numerous.

gs: I hope you laughed at that one. Everybody is in fine form this morning.

Mother of five: I was in a position to be involved in a discussion about a case of suspected BSE (Mad Cow) at one verterinary college. Yes, it was spoken of in the softest tones in the hallways and was not greatly discussed in public because absolutely noone wanted the news to spread IF IT WERE NOT TRUE, which, thankfully turned out to be the case in that instance. I have been involved in other situations involving suspected reportable (animal) diseases and the inclination is to nail down every fact before going too far up the chain because of the massive disruptions that would be triggered and, once you light the fuse, it is nearly impossible to undo the damage. If you don’t hear anything, it likely because you are now dealing with a human disease having repercussions on a massive scale and nobody wants to trip the wire unless they are 100% positive they have to. Because of these concerns, I agree with you that, if this moves too fast, the horse will be long through the barn doors before the announcements will be made. Please realize that it will likely not be due to a cover up, but because honest people need to make sure they are right. It is a huge burden for those involved and, wherever I have been in instances such as these, I have come away with deep respect and admiration for how such people are willing to do what they need to to get the horrible facts out if that is warranted. I cannot say that those in the political arena who get this information passed on to them will handle it appropriately, because I have not dealt with them, but I would hope most are also honorable (the problem may be that they are not scientifically knowledgeable enough to know how to handle the information appropriately, dealing with it as just another political issue instead). So, feel good that decent people are watching this who will do the right thing up most of the chain, but keep on the wiki because: 1. You will hear the scuttlebutt here first and may get the advanced warning you (and I) want and 2. It serves to keep all those politicians on their toes, if not completely honest :)

Many Cats, perhaps reporting the earlier results without 100% verification would serve the greater good, however. Let’s follow the algorithm: 1. The observer (WHO, CDC, etc.) collects the data and suspects from a clinical perspective that it is avian flu. They can either make known their observations or wait weeks for the lab results. If they promulgate the data, then either (A.) people have advance notice and chance to prepare, or (B.) people react negatively (panic). If they keep the data to themselves, then neither (A.) nor (B.) can occur. 2. Once they get their lab analyses back, they either determine that it is (A.) HPAI H5N1 or (B.) something else. If it is 2.(A.), then they make their announcement but have lost precious time. If it is 2.(B.), then their announcement under 1.(A.) may have been premature, but now people are thinking about the problem. It may have caused 1.(B.) to happen, but under that scenario people are still thinking about the problem. In other words, this problem is not going away. Experts say it is only a matter of time before a flu pandemic strikes. The world press is still not paying attention to this problem, because everyone is still waiting for lab results. Under this grossly oversimplified analysis, Dr. Niman is in my opinion doing the right thing by looking at and using the clinical data instead of waiting for lab results, lab results which no one can say with certainty will be accurate or timely.

De jure: I agree with you wholeheartedly. I was in a situation involving animal diseses with largely economic impacts to be considered (Mad Cow aside). In the case of H5N1, we are talking about the potential for a fast spreading human disease which could bring death on a scale previously unimagined. I would hope that some advanced warning signals would be sent. I believe that there will be people willing to speak out, at risk of their jobs, to alert us. My only concern is that such information may not travel as quickly in the standard media as it will over unofficial sources on the internet. That is why I am a wiki addict. :)

The WHO/UN gets its money from its member states. Certain (wealthy) member states have a habit of not paying their dues, and clobbering the UN with criticism and withholding of funds. I think they are a force for good, insofar as they are able to be. I have great regard for the United Nations. It is a noble concept, a great unfolding experiment, and I pray for its ultimate success, which will redound to the good of the human race.

Birds falling from sky north of Baghdad

Updated map at

http://www.recombinomics.com/H5N1_Map_2006_AfricaF.html

How ironic! Today I was driving my car and noticed a flock of birds flying and I wondered if sick birds would start doing that — dropping out of the sky. I thought “Nah, they’re probably like people. People don’t just drop dead from the flu while walking around. A person realizes they are sick and they sit down or lie down. Surely a bird would land somewhere if it was sick.” I guess they are not as smart as I gave them credit for!

I think I am thinking about this flu thing entirely too much.

niman – at 17:31 what is the source for the update of your map - Birds Falling From Sky Baghdad? I can’t find a news report on it. Thanks.

Henry: I don’t think you know what you are talking about when you accuse WHO of a cover-up. WHO works within in international system that dates back to the Peace of Westphalia, which essentially establishes international anarchy as a system (i.e., it allows no power over sovereign states). Realpolitik and power politics does exercise rules over nations, of course, but that’s not a part of the system WHO can partake of. They are a creature of their member states, cannot demand to go into a state if they are not invited, cannot demand test results, cannot release information without permission, cannot do many things you may feel are necessary. I have been very critical of them but you have no idea the constraints they are working under. They don’t control “their” reference labs and the results from those labs don’t go to WHO directly (they go first to the member state that requested them who then provides them to WHO — if they wish to).

We should be strenghtening the hands of the many dedicated people who toil in international health (for less than they can make elsewhere) and who want to do the right thing. That requires constructive criticism. I’m not here to defend WHO (there is much to criticize and I’ve done so), but there are limits to responsible criticisms and I think you are exceeding those limits. Many of us are still waiting for you to divulge the secret science you claim will reveal how all viruses (and influenza in particular) will evolve and which is the chief product of your company. If it is truly valuable to public health you must make it public or explain why not. Time is getting short and if you want to have some constructive influence on events, a good start would be to provide us with the useful tools you say you have.

And please do not use the Forum as a link fest for your site.

Birds falling from sky article

http://www.alhaqaeq.net/defaultch.asp?action=showarticle&secid=20&articleid=45705

Hear, hear. I checked out Recombinomics because Dr. Woodson gave it as a resource along with FluWikie. I have found FluWikie helpful, informative, and interesting to peruse. But I had to delete my Recombinomics because it made so little sense to me. And he has so many postings here that it starts to seem like spam.

Revere…personally, I like the “link fest”…Niman always backs up his arguments with links to more info on his website (or other websites, as the case many be)…By the way, this IS a NIMAN THREAD…so why shouldn’t NIMAN post links to NIMAN’S website???

Hmmm…Pilgrim…you, too? You are reading a NIMAN THREAD…If you don’t want to be “spammed” by Niman, don’t come to this thread….If you 2 would like to start a “BASH NIMAM” thread, I certainly would be pleased, that way I would not be “spammed” by the “bash Nimanites”

Good point, rockyman. I oughta take the advice, and I will. Adieu.

rockyman,

Henry provides no science on his site and that is the revere’s complaint. Henry provides his opinions with no science to back them up and the scientists are getting tired of it. Are you scientifically equipped to understand scientific studies? No? Henry’s links are pure self promotion and add nothing to the value of this Wiki.

Niminites: yes, we love his links, we love his posts. But why -oh - why doesn’t he give more explanation? Revere’s post puts the herculean task WHO has into perspective. We can bash them all we like, but they are the ones on “the ground.” And based on the restrictions they face, maybe they are doing a great job? Niman seems to be right about a lot of things and I visit his updates daily. But I would like to see more responsibility in his posts.

I would think someone would get kicked off the site for that kind of personal attack but you are an administrator so nothing can be done. Don’t you think a little tact is called for?

Melanie,

I appreciate your comments, but I do disagree…I just can’t understand why someone would come to a thread entitled “Niman III” and then not expect to see links and commentary from Niman himself. That would be like joining a Britney Spears local fan club then complaining when Britney herself shows up and sings a song “off key.” If you don’t like Niman, then why in the world would you come to this thread and complain about him? It is obvious that “Niman III” was created by someone who wanted to have a place to discuss Niman’s opinions. If you don’t want to hear his opinions, then just don’t come to this thread…Be “tired” of Niman in a different thread. By the way, I do have a science background and I do grasp what Niman writes (even if I don’t always agree with his reasoning).

All,

I don’t know to whom your comment is addressed, but when a scientist like Niman is unwilling to back up his claims to other scientists, I think that’s a pretty serious flaw in his work.

revere is a scientist and able to judge Niman’s work on its own terms. Are you?

Melanie – at 19:00 OOOHHH! The Niminites are about to bash you! Seriously, can you lead me to a thread here that talks about the ethics of behaviour during a pandemic? I’ve been watching the “I’m ashamed” thread and thinking it is as DeM says, “the best discussion.” The role of WHO in this, poor souls that they are, will diminish as we need to get more involved in our own communities. Luckily, mine had a BF planning meeting and cut to the quick: Temporary morgues, morgue workers, volunteer health care workers, community security workers, food distribution workers. They didn’t waste time on vaccination or Tamiflu issues. I was proud of them. But, considering that it won’t be only 1 strain of BF that simmers up, first wave survivors may have a lot more on their plate. Social isolation (as reported in Iraq) concerns me. Can you guide me to that discussion?

Is there anyone that can give us a translation of the “falling from the sky” story?

Falling from Sky Article:

Translation (Thanks Theresa42 from Curevents!):

Machine translation from Arabic:

The departure of tens of families from the regions the surrounding in Samarra for fear of the bird flu Sunday 12, Febreuary 2006

Tens of families who live at the ends of Samarra city (120 km in north of Baghdad) Sunday with leaving their regions started for fear of the spread of the bird flu disease after many of the dead migrating birds fall on the land.

And according to the correspondent, these dead birds started falling since Saturday in the times regions (20 km south of) and the castle (6 km south of) where tens of it fell between the migrating birds flocks that were passing in the sky of those regions.

And Shaiban said his drawing (28 years) that with his four children Wouzougth escaped from the times region “it decided the escape from my house to Samarra where I feel more safety after the fall of two birds in front of my house Saturday in the morning.”

And he added that “the birds that the land fell dead Gharib’s inquirer got out of their beak and appeared very thin.” And its drawing followed up “I carried out slaughter and burning of tens of poultry that I breed in my house for fear of the disease.”

From its side Mohamed Ibrahim (36 years) who 6 km in south of Samarra to the city center escaped from Castle region with company said its husband and its children “tens of birds fell a dead of unknown reasons then it decided the escape to the city for fear of the injury of my children by this disease.”

From its side the doctor Khaled Al Abbasi from the general hospital of Samarra confirmed “sending four men to Baghdad for their injury by pleasures a sharp influenza.” And he added “the saying is not possible the four was injured by the bird flu despite the sharp symptoms that appeared on them and the laboratory examination the disease kind will define.”

From its side she said by Soad Ahmed (35 years) who escaped from the times region to Samarra with her three children that does not carry except simple purposes “they watched the birds and she falls from the atmosphere and escaped with my children fearing for them from the bird flu.”

And doctor Muhammad Al-Qaisi the responsible for the veterinary laboratories in Baghdad confirmed that “the initial symptoms for the injury of the birds with a virus +H5N1 the exit of liquids from the birds mouth and the redness of its head which calls for holding my interior examination for the determination of the injury accurately.”

And the health headquarters has carried out in Salah Ad-Din’s governorate sending medical groups for the verification of the order and holding examinations to the birds the dead and taking samples from them for holding the medical examination and defining the disease kind are as it declared a source from the governorate council.

And the source added “we carried out sending four medical groups for seeking the disease cases that led to the fall of the birds and their tunnel from them two teams to Samarra and a third team to the stage (205 km in north of Baghdad) and fourth to the regions of Waldgil country in south of Samarra.”

And the source pointed to that “the regions that the health groups headed for it represents the migration line to the coming birds from north of to south of the country.”

And the first death case by the bird flu disease has happened in Iraqi Kurdistan where she was recorded and Vatan is two certain by an influenza the birds and the entrance of five patients suspected by their injury with the disease took place Wednesday at night to the hospital of the general As-Sulaymaniyah what the number is raised the total for the injuries the suspects to ten in north of Iraq.

As a single person was dead in Amarah (265 km in south of Baghdad) by the bird flu disease symptoms but till now results did not appear the laboratory examination of samples of Mohannad Radi (30 years)’s blood that was fond of the aviculture.

While enter the building hospital five patients all from Radi’s family members after on them symptoms appeared are a similar to the bird flu that claimed the life of their relative. And the laboratory examination results of samples of a blood did not appear these five until now as he reported a medical source in Al-Imarah city.

I think I”ve figured out a major source of the many rants against Niman by scientists and other web authors: jealousy.

Since this appears to be a lively thread, I thought I’d post this question here (Niman probably has an opinion :)

This is a quote from The TimesOnline (UK):

“THE deadly strain of H5N1 bird flu has been detected in four European countries, carried by swans driven south by freezing weather in northern Europe.”

If these swans came from NORTHERN EUROPE, how did they carry the bird flu with them (since the bird flu has not been reported in Northern Europe)?

Thank you for the translation. I tried but could not find an online translator that could accomodate.

Montanan,

Let me see what I can do while I’m being beaten about the head and shoulders by the Nimanites. I’ll post a link when I can find it, I know we’ve had this discussion.

giraffe, have you ever seen a machine translation from a document or newsarticle in your field? No? It’s usually gibberish. That’s what Henry is relying on. I sure as hell wouldn’t.

…”revere is a scientist and able to judge Niman’s work on its own terms. Are you?”

Yes, another man of science, thanks.

Cheerio! 007

Seems to me that Niman is presenting quite a lot of raw data on his site – data that is not easy for others to get. His map plots are providing data for all to interpret as they see fit. He is presenting much information about the way in which this information is used and analyzed by a virologist. Apparently, he is constructing some type of a computer model (doesn’t take a rocket scientist to figure that out) Currently it is proprietary – OK that is the American way. What he is constructing is not going to save the planet, it might help with forecasting if you listen and use it.

Sure, he is off base in some of his criticisms, or is he just complaining like the rest of us.

Back in the 70s I wrote some of the first computerized software for diagnostic testing in psychology / psychiatry and ran into a s-storm that I never anticipated. We had all of the publishers locked up, great software, and 100s of thousands of customers including many government agencies. Much of the stuff we had was in the public domain and I had no trouble making it and all sources available to my colleagues. Next thing I knew there were people trying to take my license, my job, 80% of what I made forever, and on and on and on. Niman is doing a better job than we did. You need to get the public’s attention and he seems to be doing that. I basically left the field because of the pressure from big business (some of which is located in universities).

If you are going to complain about his approach, do a better job. You construct the model and put as much info out there as he has. You construct the hypothesis, and suggest how to test it. Conduct the study, build the model and then give it away. As someone said on another thread – Come on get real.

Melanie, I am sorry you missed my point. I was suggesting you soften your words but this is your place and you sure don’t have to. I come here for info not debate so I would rather not get into a spitting contest. I really do appreciate what you and your friends have put together here.

So now Babelfish and his brothers are part of the Niman conspiracy?

Joel makes a good point, who (tongue and cheek) is out there to put up their theories and stick their collective necks on the line?

All,

I’m not a big fan of spitting contests, either, but letmetellyou, moderating this place, where the motives of the moderators get impugned with some regularity, is a bit of work. After I’ve been bashed for the double digit time in one day for making a hard call, I get a little cranky sometimes.

You guys get this place for free. I’m the one that set it up and paid for it for you and never asked for a dime. Do I get any gratitude…..I think there is a Woody Allen movie in here somewhere.

Melanie, I never realized until now, that you set this up. Actually, I and my family are grateful for the information and the heads up in monitoring this world tragedy unfolding. Hats off to you, Dem, pogge and the rest of the gang. Eternally appreciative… Thanks.

rockyman wrote:

I just can’t understand why someone would come to a thread entitled “Niman III” and then not expect to see links and commentary from Niman himself.

Do I need to point to the numerous other threads Dr. Niman has started so he can post links back to his own site? You don’t know the whole context. If he’d stick to one thread at a time, it might not have provoked the comment in the first place.

Let’s stop bashing “Dr. Strangelove” Niman and get back to the multifaceted, really juicy stuff. It seems very strange to me that there can be “leaks” from top-to-bottom in the British Government and the United States Government, but where are the leaks from WHO? Where are the noble whistleblowers of malfeasance and chicanery? And please don’t tell me there are not any such instances of wrongdoing regarding WHO’s handling of this avian flu steamroller.

The United Nations is a rotten apple, and even though WHO may be the shiny part of the apple, they are still rotten underneath. Scientists and technicians can be compromised just as well as any of us. If they are afraid to speak up given the stakes in play, when would they ever speak up? Contempt, Contempt, Contempt.

anon 33: I was not happy about taking Henry to task as I did. But I felt compelled to do so for several reasons. He isn’t at all reticent about casting aspersions on WHO or anyone else that contradicts his speculations and therefore should expect someone to call him on it when such is warranted (and it is warranted here). And because he has been touting his proprietary set of rules that he says will enable us to predict the evolution of the flu virus (not an unimportant thing for us to know, wouldn’t you say?), but never tells anyone what they are. Thre can be no excuse for holding back if he has something. Otherwise, time to hold his piece. As a scientist I want to see the science. He has so far refused to provide it. That’s the end of the story for most of our profession. You may call it jealousy, but that’s the way we work.

Moreover, as we get closer to a difficult situation, it will become much more important to be careful about our speculations. Henry is not careful. Maybe some will turn out to be right and that’s great. But many in the past have turned out to be wrong or were never substantiated. In an atmosphere of high public anxiety this can lead to some very bad decisions on the part of innocent people.

As to the link fest, we allow some of that on the wiki but not to excess. I have linked to Effect Measure on occasion. But we both have our own sites and you can go to them if you want. We have banned IP addresses for doing site building on the wiki and we will continue to do so. If it is worth discussing — and not just holding forth about — then the text can be posted here so others can react to it. Henry doesn’t allow comments on his site which is neither a blog nor a wiki. It is his site, purely and simply. The wiki is for dialog and sharing. Links and commentary from Henry are welcome and encouraged. Notes to “see my site” are not. This is a Niman thread. It is NOT NIman’s thread.

Eric,

This is a work of public service by the posters, pogge and the moderators. Everyone who posts here is a contributor to “the wisdom of crowds,” which is what we are collecting here. Wikis are for you, by you.

Another rant: Niman is unprofessional. You know I heard that many times from colleagues, most of who did not know that I sat on the ethics board! Colleagues (not the general public) challenged my audacity, unethical behavior, and arrogance to construct and MMPI analysis for a personal computer in the face of software available from, of all groups, Roche.

I learned that professional jealousy is rampant and there are people who can take on the mantle of morality and righteousness who are the last people to assume such a position. Watch yourself – are you one of those who instead of encouraging new and innovative work is protecting their professional butt?

I found that some of my most vociferous critics were people who were making huge amounts of money based on antiquated laboratory systems. Consider the source, which here remains unnamed far too often. It is easy to to take pot shots. Niman is “out there” working. What the hell are you doing???

Some of the people here are really starting to get my dander up. Oh by the way, I am a distinguished professor of research at my small Midwestern university. So before you consider telling me how science works – consider the source.

Melanie, I really feel upset that you are having such a bad day. I am a softie for anyone in distress and I can see how much you are and I’m sorry. That said, I do want to make it clear that if you carefully read my posts, I am not attacking you. I felt you were attacking Niman personally and I felt bad for him since I think he is a sincere man. (Insert Rodney King quote here). I thanked you for your work in my last post and I really meant that. I direct people to this site all the time and believe that you and your friends could be responsible for saving my family’s life in the future. Thanks again and I hope your day gets better. I know, I know, it would if I went away.

It’s not my style to bash Henry Niman or anyone else. As I’ve said elsewhere, my official position is that sometimes he’s right and sometimes he’s not. pogge actually had the best crack at it from my (moderator’s) POV… he needs to follow the rules like anyone else. That’s all. No posting a new thread every time there’s a new post (w/link) at recombinomics. Promise to post an update about the prediction, and I’d expect that promise to be kept. I’ll be happy to see it, here or at his site.

revere is correct about the ‘no comments at recombinomics, comments here’ thing. In fact, niman has gotten into a bit of trouble at two other BBs I know of for various and sundry things about comments. So, JoeW, it’s not about ‘my creds are bigger than yours’. It’s really not. Nor are his POV being ‘supressed’ in any way (they can’t be.,.. they’re everywhere). Henry’s welcome here, I have verified it’s the real niman, but I’d hope the same rules apply to him as to everyone else.

JoeW,

I’d be happy to have you provide me with any actual science Henry’s posted here or anywhere for that matter. When I follow his links, I get opinion. Replicatable studies? Gee, haven’t seen one yet.

When I think of Dr. N…I envision S.R. Hadden in Carl Sagan’s Contact. Knows his stuff…ruffles some feathers (euwww…bad pun…)…likes the controversy.

“Science” consists of “data,” and “analysis” to generate “theories” or explanations and predictions. There are many ways to do that. In the beginning, we describe the phenomena under consideration in the context of the data that are available. Review Niman’s site you will find lots of data and plots (maps) and descriptions of how it is analyzed. There are different ways to conduct “science.” Do not fault the man for not following your preferred model. Take him to task for his explanations, show a better explanation until you can develop a theory that predicts the phenomena better than he does. He has made predictions if you read his prior posts. He has couched them in vague terms and he is contributing in his own way.

As someone who agrees with Dr. Niman on some things, but not others, I’ll take a chance and stick my neck out.

I agree with the moderators that Flu Wiki should not be used to advertise Recombinomics. If Dr. Niman wants to make a comment he should not start a new thread on a subject that already has a thread. His links to Recombinomics should be used judiciously and only to provide detailed information that he cannot easily put into a post at Flu Wiki.

I still agree with Dr. Niman about the WHO. I think the Director-General is deliberately witholding data. I agree that many countries are covering up cases.

I am agnostic about the importance of recombination in H5N1 evolution. However, he did appear to make a specific prediction about a mutation which turned out to be true.

Some of this unpleasantness could have been avoided if Dr. Niman would learn to argue more politely, but I fear he has been bashed so many times its difficult for him to contain himself.

Revere, Melanie, Dem from Ct and other moderators: I have been having some nagging doubts about the reliability of many of the posts I’ve seen here, especially after learning that Niman was more or less tossed out of a couple of other blogs, and has been associated with a few “controversial” issues. Of course, none of these things mean Niman is always wrong or his assertions always baseless. Nonetheless, I was very relieved to see your criticisms here of Niman. They answered all the questions I had about fluwiki in general. Thanks so much for restoring my faith in your site’s credibility and for providing what may yet turn out to be some of the most valuable ‘net real estate in existence.

Melanie. Of course you are right. Joe W I would like you’re comments on Tram’s post at 1.14 pm on the thread…Only two mutations away from pandemic.

Gosh, I went away for a bit and come back to see I am in trouble for saying thank you for the translation. Not sure what I did…..

In the interest of straightening at least one aspect of this great big ‘is WHO covering-up’ debate, I looked up the WHO site. Guess what, they have a lot of material that will give you a clue as to whether or what to accuse them of.

This one http://tinyurl.com/dgtaj WHO guideline for global surveillance. On page 4, ‘reporting and dissemination of information’ you can find detailed guidelines on how exactly and how often member states should report. Two things to notice: first is the word ‘request’, which means that they can’t do shit if the states don’t.

Second, take a close look at the templates especially Annex 5, (pg 15) template for case report form. Notice how much detail is laid out.

Did Turkey fill in these forms? I should think so. Did they put in onset dates, etc? I don’t see why they wouldn’t, particularly as you don’t know you need to cover up a cluster when you don’t even know you have a cluster yet. (Clusters are by definition discovered when there are sufficient cases and with hindsight. They don’t walk in the door hand-in-hand and say, Hi, we are a cluster.)

So if the WHO has the dates, did they decide to not publish? Or did Turkey tell them to not publish? It’s hard to tell, could be a bit of both. However, given that Turkey at the time this was unfolding was in desperate need of assistance from the WHO including shipping in tamiflu, I don’t think they have a lot of leeway in making decisions like that if the WHO insists on disclosing.

giraffe – at 20:46

You did nothing wrong at all. Machine translations can be spotty. Melanie was just pointing that out. In fact, in many of his posts at Recombinomics, Henry points out the same thing. He’s working with what he has, but they’re not always reliable.

I decided not to post after one of moderator’ comment on my post. If you continue to implement “Ptolemy” rules and regulations, I am afraid other people will stop active participation.

Eleanor Holmes Norton:

The only way to make sure people you agree with can speak is to support the rights of people you don’t agree with.

PS Dr. Niman is a fresh air in the ivory tower

Tom DVM,

I’ve looked into the science and I’m blowing hot and cold on this depending on whom I talk to. In the larger scheme of things, I think it is playing with statistics. Is the virus going to evolve or not? Where do I want to lay my bet down? For me, its in preps. Dem and the reveres have made other bets.

informatic – at 20:54 you can’t please everyone all the time, whatever you meant by “Ptolemy” rules. Sorry if you’re offended.

Melanie. In my opinion, and it is only my opinion, there is death, taxes, and this thing is going to mutate. I hope and want to believe in Dr. Butcher et al arguments, I just can’t see it…and when it goes I’ve come to the conclusion that it is going to be very bad.

Many have talked of the importance of this site and I agree but the real value will be at some point in the future when the inevitable happens.

My, but we are a testy group today. I’ve been here since November and haven’t quite seen anything like this before.

Perhaps as the events are speeding up toward the end we all fear, our stress is getting a little more difficult to manage.

The moderators are people, too, each with their own opinion. If I criticized someone would they go away? I don’t think so.

Maybe someone should start a thread on meditation and relaxation techniques. Could come in handy in the days to come…

I think of the information given out by Niman and its reliability the same way that I think of information given out by WHO, Webster, Purdue, Osterholdm… you get the drift.

Each one of these people or organisation has far more expertise and access to data that I do not have. However, every source has its drawbacks and limitations. Personal agenda distorts the data or interpretation no more nor less than political agenda. Such agenda or vested interest can be related to money, fame, expediency, fear, ignorance, even a mild degree of martyrdom sometimes.

My job is to notice all these factors and then carry on with my own evaluation of the situation (which is probably just as flawed, but is better than not having any.) It is understandable to get upset if you think someone is misleading or covering up or manipulating. On the other hand, us being mature adults, I wonder whether it is worth spending so much energy on blasting or defending one guy, especially as much of what he writes is not something we can prove any time soon.

I like reading his posts. I like his maps and sometimes his explanation of the mutations, when I can understand them. But I remind myself that what he writes is one hypothesis among several possible ones.

Anastasia,

Do your best.

Yes, there is a lot of fear here. And it is warranted. It might be that we are staring down something which is unprecedented in human experience. Or maybe not. Much of the psychological reactions are predictable, but, as Freud said, the human is given to “polymorphous perversities.”

The subject is life and death and so we will wrangle about it. That’s to be expected, and this place would be a bloodless list of things to buy at Walmart if we didn’t. I sort of enjoy the shear exuberance of the discussion. We’re alive, dammit, and that’s something!

Does anybody remember S. R. Hadden in Contact? :)

I have been following wiki for about 2 months now and find the information to be helpful in prepping for the coming pandemic. I find myself fascinated by Niman’s scientific reasoning and with difficulty at times, can follow his research. Objectively speaking the last forum additions sound as if everyone is feeling a little anxious, overwelmed and powerless in the face of an advancing medical nightmare. True, we don’t know if Niman is correct in all his scientific reasoning or if some are simply conjectures. However, I think he is trying to present the facts as he interprets the information he gathers. This is all being done to help people utilizing the wiki site to plan and follow closely the advancing flu. Whether this is being done for our benefit or his glory is a mute point to me. The fact is that the avian flu is coming to the United States on its own timetable and this seems to be increasing in momentum. I sense there are many strong personalities on this forum. All with much to offer each other. Yes, this is a Niman thread and I for one see no harm in his threads he adds to his comments. I find they often explain his statements made here without him having to reiterate info he has presented on his own website. Going to his website is a choice whith his commentary. I will continue to read and utilize all the information presented here. All of you have given me information to think about and decide if I agree or not;if I can utilize it in some way to benfit planning for both myself and my family.As a RN who works in a children’s hospital I can assure you there will be no room at the hospitals when the flu comes. We have no beds now in our day to day admissions.Vanderbilt is a huge medical institution and even now with RSV(severe resp. illness in babies) we run of of isolation carts. Our pediatric ICU’s are full always. I would like to know if anyone knows whre I can purchase IV fluids. I read they are OTC in Canada but have been unable to locate a website. Any ideas? Dehydration will be a major player in all of this-if the multi-organ effects don’t kill you anyway…. VandyRN

Vandy, I have no problem with you reading Henry. Please read everything you can find. But know what you are reading. The other editors and I have a problem with Henry trolling for hits over here. If he has the goods, people will find him and he doesn’t have to be a link troll over here. He adds nothing to our discussion.

Tom DVM:

Quoting Tram “Niman, you are making assertions based on rumors and speculation. Based on that, you are no more credible than the WHO. All one has to do is visit your site and read the archives. It is full of rumors and speculation and most of which has proven false. Moreover, says Alan Hay at NIMR, only some of the boy’s viruses had the mutation. Such mixtures can arise during an infection, as the virus mutates and strains that bind human receptors better emerge, says Mike Perdue at the World Health Organization. But he says “we’ll only know it means something if we see it in a cluster of human cases”, where it has been selected for because it eases spread among humans. But this has not happened so far – Fatma’s virus did not carry the mutation, says Hay, meaning she did not get it from her brother. And all human cases in Turkey can be traced to sick birds, says the WHO “

Not sure what to make of this. It is suspicious, but given the slamming that Niman takes I would certainly want to hear more. Apparently Niman did not have the data. That would be my assmption. Did he step out too far? — I don’t know. What has transpired since then?

Dem, I did not make comment about the quality of the translation at all. In fact, I am not even part of this arguement…for or against. I only wanted to know what the article said and had attempted to translate it myself,but the sites I normally use did not offer this language. I understood the main idea of the article, but not every detail. This is probably not very nice…but I just wanted to know if Dr. Niman meant that they were literally falling from the sky. No judgement whatsoever in my quest. I admit, quite freely as a matter of fact, that I am not qualified to make a qualitative judgement here. I listen….err read…and try to understand. That’s all. I most definitely do not want to get on Mel’s list either. :)

Does it really matter at all what the WHO says or does? Does it matter what the level of preparedness is? My understanding is that 10 or so years ago, if we could have identified and killed (culled) the index cases of H5N1 in China- we could all be worrying about our retirement accounts or crappy cars. This virus looks unstopable to me and probably has been since 1997. It is going to do what it is going to do. It does not care about us at all.

Now, what Henry Niman is doing could make a difference to all of us. My understanding is that our salvation, at some medium/long term point is the production of good vaccines. Good vaccines means prediction of the virial sequence, producing and distribution of it before the new viral itterations.

I think that is whatr Henry is on about- getting one or two steps ahead of the virus, so as to check it- I don’t think that checkmate is really on the table. We are going to have to figure out how to live with H5N1.

SO, in my opinion, what WHO says or does will not really affect any of us one way or the other, but what Henry Niman, and other researchers could affect us alot- but then again, maybe not.

Just wishing for the best and learning sterile technique.

JoeW,

Niman has a track record going back to SARS and it is all in his archives. You might want to take a look.

Afaik, niman suggested that WHO and/or whoever was looking for mutations were using egg based cultures, which were selective for not having the mutation. niman further suggested checking other (better) culture medium which would select for the mutations in question. I don’t know the science to say who/WHO was correct.

I haven’t seen anything else in terms of data.

clark, each is contributing in their own way. Having investigators on the ground is a vital function, as is coaxing the national health agencies to act, identifying where weaknesses are, following up rumors, etc. WHO’s work is invaluble and is not being done by anyone else.

This isn’t or shouldn’t be either/or.

Joe W. Thanks for the comments. Sorry, the comment from Tram was from 13.14 titled..A few examples of rumours and speculation from Niman’s website on the thread…Only two mutations away from pandemic.

Melanie: Do you realize that you are doing what you implicitly accuse Niman of doing? Time for bed – good night.

…”He adds nothing to our discussion.”

I find Henry adds a great deal to the discussion. In fact, lately he has been THE discussion. See?

Cheerio!

007

As far as I understand Henry, he suggested that maybe the reason the WHO ref lab (which isn’t WHO’s) didn’t see the mutation is that they cultured it in eggs instead of MDCK or Vero. Maybe. I don’t know what they cultured it in. Nor as far as I know does Henry.

Regarding Clark’s point, it is the point I was making, too, except that Henry hasn’t told anyone how to make a vaccine (that I am aware of). If he knows, time to tell us. Or tell SOMEONE. Don’t you think?

I think it does matter what WHO says and does because it affects (literally) billions of people.

I don’t know where Naborro’s “two mutations from a pandemic” comes from. He doesn’t know that nor does anyone else. Maybe it’s one mutation. Maybe even zero. Or maybe ten.

As far as I understand Henry, he suggested that maybe the reason the WHO ref lab (which isn’t WHO’s) didn’t see the mutation is that they cultured it in eggs instead of MDCK or Vero. Maybe. I don’t know what they cultured it in. Nor as far as I know does Henry.

Regarding Clark’s point, it is the point I was making, too, except that Henry hasn’t told anyone how to make a vaccine (that I am aware of). If he knows, time to tell us. Or tell SOMEONE. Don’t you think?

I think it does matter what WHO says and does because it affects (literally) billions of people.

I don’t know where Naborro’s “two mutations from a pandemic” comes from. He doesn’t know that nor does anyone else. Maybe it’s one mutation. Maybe even zero. Or maybe ten.

We (the moderators) and I, personally, are not trying to shut Henry up. He comments regularly now at Effect Measure and he is welcome there. There is a place for everything.

Yes, I wondered about Nabarro’s comment too. I was hoping someone else might have some info on that. Seems not. Oh well…

Hi Dem- I was not bashing WHO- just the opposite. Reminds me of relationships; when the partner has had a shitty day- and I get it in the neck- you know heads I win, tails you lose. Everything you say or do -or don’t say and don’t do is WRONG.

My reading of the situation is we are all (if we have been paying attention) worried. (I’m worried). We get worried (about us and ours dying) and we get shitty. We lash out. We lash out at whoever is around (the nearer the better).- so we lash out at each other. If we don’t lashout at each other (Henry is one of us)- then we lash out at WHO or the UN or George Bush, Big Pharma or what ever.

The problem is, no matter how sharp our sting- how quick our wit- it is pointless.-

because it is the H5N1 that is the problem- and it doesn’t even know we exist. It has hardly even tasted us. It is much more into birds right now.

anon_22: You seem to think that WHO is withholding data, too, especially in regard to the Turkey clusters. It is hard to come to any other conclusion. Why isn’t some underling within that organization stepping forward to tell the truth? Why isn’t there somebody in the WHO putting the public’s need to know ahead of their paycheck or position, especially in this matter of extreme gravity? I read about leaks every day from about every type of governmental body and NGO, but here we have WHO, the “stone wall” of all “stone walls”. And you know what, it stinks to high heaven.

There is no way to evaluate Dr. Nabarro’s statement without seeing the sequence data. Even then, it might not be obvious. This is one of the maddening things about the WHO/UN. They will make very signficant statements on the basis of data that only they have access to. This type of behaviour is absolutely unacceptable, especially on a matter of such importance.

As regards their constraints. I don’t buy it. If they have important data that they are being prevented from releasing by an affected country, then say that. You can’t praise a country for its transparency and cooperation on the one hand and then claim that country is preventing you from releasing critical data on the other hand (perhaps subtly, with some well-placed leaks). Typical sociopath double-dealing, IMO.

I have no doubt that some countries are not cooperating fully and that WHO investigators are having the devil’s time getting their hands on some of the samples. But, there is some very old epidemiological data from countries like Viet Nam that never were presented properly by the WHO. How do I know? Because it was in the press. And how did I find all the right press reports? By reading the Recombinomics archives. Were they accurate? Yes. How do I know? Because descriptions of some of the cases were subsequently published by others.

Anyone who doubts that the WHO is providing incomplete information please read this paper. Then go to the WHO situation reports and see if you can abstract the same information. Some of it will be there, but some will be missing. Especially the cluster information. I am trying to piece together all the cluster information here?. Believe me, the WHO does not make it easy.

Med Maven, I’m sorry but my expectation of WHO is far lower than yours, has been for a long time.

oo7,

And exactly what is it that Henry adds to the discussion beyond his opinions, which aren’t worth much more than mine or yours?

anon_22, I hope you will read what the reveres have to say about WHO, which is about the most balanced comment I think we’ve had here with more facts than most.

We all know and understand the WHO and the UN and their track record very well. Both Medical Maven and Monotreme and all others who have made comments in this respect are correct. I expect nothing from the WHO. Nothing they are doing or going to do is going to protect my precious family or the precious families of my colleagues on flu wiki. I will ignore anything this agency says in the future because any information they provide, they provide without any scientific evidence to back it up. WHO is a political body not a scientific body….and we fool ourselves to think anything else at this point.

Comments on birds falling from sky in Iraq

http://www.recombinomics.com/News/02120603/H5N1_Sammara.html

I step out to go to dinner with my wife and come back and find this. It’s no wonder someone started a thread about being addicted to this website…you almost have to be or you’ll miss something. It seems the information on this virus shared by diverse sources from around the world is mutating faster than the virus (oh, sorry, I meant to include “recombining” as well). If everyone took a step back and looked at their comments, they would see that they each hold a piece of the puzzle, and by a puzzle piece’s sheer nature, it must be different from all of the rest. Moreover, it can’t be argued that every contributor comes from a different background with different experiences. JoeW shared some personal information as to why he feels as strongly as he does. Melanie shared some information about her personal efforts at keeping this site running. Again, take a step back and try to glean some little tidbit of information from someone with a different point of view. I’m just trying to put the pieces together. You have to admit that more correct predictions than not have been made on this site about what the virus will do next. It’s almost like that TV show where the guy gets the morning paper a day in advance, then tries to go out and set things straight before they happen as printed. I don’t agree with everything that Dr. Niman does or how he does it, but thank God for Dr. Niman anyway (whether he be right or wrong). He gets me thinking about how things might happen. Also, thank God for Revere, pogge, DemFromCT, Melanie, Anon_22, Monotreme, Racter, informatic, dude, and all of the other teachers, professors, doctors, vets and others that contribute to this site (I hope the phrase “thank God” is not too contentious?) The only reason I can think of that someone else hasn’t chimed in this evening is that it’s bedtime in Germany? By the way, does anyone know whatever happened to Oric? It would be interesting to see what he thinks about what is going on in Turkey right now.

Melanie, if Niman’s posts do not add value, why are so many people spending so much time debating this? Not just here but on other forums as well. Clearly there is no consensus. So your statement that he doesn’t add much is nothing more than you opinion. Given that we don’t seem to be able to resolve this issue, perhaps it is best if we let people form their own opinions without having to wade through so many pieces of opinions on Niman’s opinion, then opinions on other people’s opinions on Niman’s opinion. Life is too short for that.

whether it’s WHO’s fault or the countrie’s fault that “invite” WHO, the situation is unsatisfactory and should be improved. The data comes late, if it comes. Niman is faster at least. And speed is important, everyone agrees here AFAIK.

WHO could make preliminary, non-official states, marked as such. WHO could post here or elsewhere and answer questions.

JoeW—As a scientist, I wonder how you can quarrel with anyone’s questioning of unknown methods. This is not the type of thing where we can say “oops” later on. As you know, this is a pretty serious matter. Niman may be doing good work—or he may not. Nobody knows because he won’t reveal his methods, assumptions, etc. I read Niman’s posts everyday. I appreciate his vigilance and it’s invaluable to have someone like him standing guard. He is the antidote to the WHO. They’re are the liberal left and the conservative right of avian flu. (Just a thought—but hasn’t the WHO given a whole new meaning to phrase “political science”)

Can you really expect everyone to accept his pronouncements out of hand?

Monotreme:

The following bit of “cheerleading” is amost surely not necessary, but just in case it might help:

Looks like the work you’re doing (referenced at the end of your 22:11 entry) is quite laborious. But it is something that, at you obviously recognize, needs to be done. Surely MANY people are eager not only to have ready access to the data you are assembling but also to know your interpretation of it.

revere, The complaints about WHO covering up the onset dates and relationships of patients in Turkey have been laid out in detail. They are quite specific and quite verifiable.

The nonsense about S227N only being in the index case that you posted on your site is also pretty silly (which is why it wasn’t posted anywhere else). If WHO has data to back up the statement (with PCR data or H5N1 islated in mammalian cells, they should say so).

Qinghai strain hadn’t caused in confirmed H5N1 infections or deaths in humans until Turkey. Now WHO is trying to say te key polymorphisms (which increases receptor bnding affinity for human receptors) disppeared?

You published teh nonsense. Is that what you believe?

As far as the two “mutations from a pandemic” are concerned, it is quite clear that the reference is to positions 190 and 225 and based on a recent paper on the 1918 pandemic sequneces and screening with a glycan chip (by Ian Wilson at Scripps).

Of course WHO has no idea when or if the changes would happen because they think all such changes are “random mutations” and can’t be predicted.

The flat earth society is alive and well and are still spinning stories to try to explain away S227N, which was quite predictable

http://www.recombinomics.com/News/10220501/H5N1_H9N2_Recombination.html

came here looking for answers I could not get from my employers, colleagues or professional leadership. I have shared, what I hope is helpful opinions, resources and facts. I believe I have found valuable information and alternatives that would be useful for responding to the medical aspects of the coming pandemic. The small group of RTs I started working with on pandemic response in September is no longer communicating, (or responding to mine), HHS has only contacted me once, (after repeated inquires) and my professional organization won’t acknowledge my existence. Once you go Wiki, you can’t go back. Everyone here takes panflu very seriously, but no one out there takes us seriously. If you contacted my people and told them the things I have said here, they would probably say, “well, his tin-foil cap doesn’t go all the way to the top, If you get our meaning”. I would love an open debate with MSM (medicine) on their “plans”. I would love to debate sending twenty-year old SNS technology to fight a 21st century killer with instructions that might as well be in Klingonese. We can’t get in “out there” and they won’t come in here. Here, for the most part, all that we believe or suppose remains un-validated. I can live with being right or wrong. It’s the self doubt that is killing me.

Henry,

I find it quite fascinating that all of your citations link only back to you. Most scientists cite studies other than their own opinions and some scientific studies, of which I notice you have none.

Thanks ssal. It is laborious and I can’t believe no-one else has done it. I keep thinking somewhere there must be a complete record of all the clusters. If you find it, please let me know. The paper I cited is the best compendium of clusters I have seen, but even it was incomplete.

I want to make clear I am not an epidemiologist or a virologist (although I have worked with viruses in the past). So, I’m not sure how valuable my interpretation is. The most important thing for me is to make the cluster data available so that everyone can interpret it for themselves. However, I will say that my opinion, for whatever it is worth, is that H5N1 frequently spreads via close contact. I base this hypothesis both on the cluster data on the cat studies that show horizontal transmission. In my mind, H5N1 is currently as dangerous as Ebola and may spread in the same way, ie, close contact with bodily fluids, perhaps blood or diarrhea. For this reason, I think it is vital that Africans be warned of this possibility as some of their funeral rituals have amplified Ebola and Marburg outbreaks. I am very concerned that the Director-General of the WHO has not warned them of this possibility.

GS, Exactly, lets get an e-mail by the moderators/creators of this site and released to the press which requests that WHO have a PR, scientist, public figure, etc. charged with the job of coming on this site and answering questions on a regular basis. If they refuse, give press interviews about what you get back etc. CC it to every member of the governing board of WHO and persons/organizations of interest. It is way past time for WHO to do more for the world. We can’t help it if their economy is damaged by this. Every nation state has a responsibility to the world community. Lets shine a big light on this.

I thought I would take a moment from figuring out if Niman is prescient or flagellant and ask if anyone besides me…notice how easy on the eyes Tara Smith of Atiology is…?

There how is that for a controversial post….could not help myself.

Monotreme, what you are saying about body fluids and Ebola and this present virus is very important. Can you start a thread and address this issue in particular, so we can untangle this from the other raging discussion that may go on forever and not lead anywhere? Much thanks for your contribution.

“Nothing they are doing or going to do is going to protect my precious family or the precious families of my colleagues on flu wiki. I will ignore anything this agency says in the future because any information they provide, they provide without any scientific evidence to back it up. WHO is a political body not a scientific body….and we fool ourselves to think anything else at this point.” -TomDVM

How about Niman?:

A few examples of rumor/speculation from Nimans website:

-Myocarditis Outbreak in Sri Lanka the Start of a Flu Pandemic? … A bird flu with a tissue tropism for cardiac tissues cannot be ruled out without testing, which has not been mentioned, even though the number of cases has grown to 170 and now affects health care workers, a major red flag signaling the start of a flu pandemic….Pandemic flu monitoring worldwide has moved beyond scandalous. (Feb 2005)

-195 Bird Flu Cases in Quang Binh? (March 2005)

-Is Ebola-like Illness in Angola Really Bird Flu? (March 2005)

-Reports from Chinese language papers detail over 200 suspected infections in over two dozen locations in Qinghai Province. In the most affected 18 regions, there are 121 deaths, generating a case fatality rate above 60%….Even if only a small fraction of the deaths are H5N1 linked, the cases would move the bird flu pandemic stage from 5 to the final stage 6, representing sustained human-to-human transmission of H5N1. (May 2005)

-The above sequence of events appears to confirm the start of the 2005 bird flu pandemic. The dates above coincide with media reports indicating that the Institute of Hygiene and Epidemiology in Hanoi had collected 1000 serum samples from people and animals in northern Vietnam. These samples would seem to have included samples from the outbreaks in Quang Binh in the central highlands, as well as the northern Vietnam clusters in Thai Binh, Haiphong, and Quang Ninh. Media reports of these outbreaks strongly suggested that these samples would be positive. (May 2005)

-The latest data appears to be moving the pandemic to phase 6. Third party reports from the western provinces of Qinghai and Xinjiang would also indicate the pandemic there has also moved to phase 6, and the H5N1 there may be more virulent than the version in northern Vietnam. (June 2005)

-This H5N1 is silently spreading mild disease in human and asymptomatic infections in poultry, which would move the pandemic to phase 6. The seeding of the human population with H5N1 (June 2005)

-The die-off of geese in Georgia (USA) are ominously similar to the Qinghai bar headed goose situation in early May. (July 2005)

-An 18 nucleotide region of H5 is found in the Ebola env gene, signaling the exchange of genetic information between H5N1 and Ebola (the sequence is specific for H5N1 isolates). Variations in sequences between Ebola or Marburg strains has been noted and Ebola like other viruses can evolve rapidly via recombination. (July 2005)

-115 Symptomatic Zoo Visitors Seek H5N1 Treatment in Jakarta (Sept 2005)

-H5N1 Cluster in Samerang Raises Phase 5 Concerns…..These growing clusters, and clusters of clusters, signal a pandemic phase 5, which is getting close to the final phase 6. (Sept 2005)

-H5N1 is currently acquiring mammalian polymorphisms, which is why several of the mammalian polymorphisms in the 1918 H1N1 pandemic strain are found in H5N1 isolates from Vietnam and Thailand…….However, the 1918 pandemic strain was not an avian strain. It was a recombinant between a swine virus, like the H1N1 classical swine virus from Iowa in 1930, and an H1N1 human virus, like the WSN/33 virus from a human in London in 1933. This observation had been made previously, based on the published sequences of five of the eight 1918 genes. (Oct 2005)

-The above translations from two media sources in Thailand clearly show that there is a raging pandemic in the country that is being under-reported. Until last week Thailand reported no human H5N1 cases, even though there were over 1134 suspect cases and the sequence of H5N1 in 2005 was very similar to 2004 when there were human cases reported and additional lab confirmed human cases that were not reported….These media reports are far more informative than the WHO official numbers, which are simply not credible. (Oct 2005)

-Boxun is reporting that there have been 77 H5N1 deaths in Liaoning Province. Many of the dead were outside workers brought in to help cull the birds. The above list includes the names, ages, and origins of some of the deceased workers. All are listed as dying from H5N1 and being cremated…..If the above numbers are accurate, the level of transmission of H5N1 from birds to humans would be markedly more efficient than reported for outbreaks in other countries such as Vietnam. (Nov 2005)

-Fatal H5 Infections in Farm Ducks in Abottsford British Columbia?…Finding dead H5 positive dead ducks on the Abbotsford farm raises the possibility that in addition to LPAI H5 from North America, there is H5N1 from Asia in British Columbia. (Nov 2005)

-139 Confirmed or Suspect H5N1 Cases in Turkey (Jan 2006)

-162 Admitted H5N1 Suspect Cases in Northern Iraq (Jan 2006)

-Most H5N1 Cases Now Linked to Human to Human Transmission (Jan 2006)

Since some people commenting on this board have some problems with data analysis, I’ll throw out some tips. Data usually comes in hard and soft forms. If you look at the hard data, you can come up with some pretty solid rules and then these rules can be applied to the soft data. Many of my commentaries are based on rule violations and are designed to help the reader analyze the data, both hard and soft.

A good example is the maps on H5N1 confirmed and suspect cases. I created the maps not to show where H5N1 was, but rather to show which countries were withholding information.

As has bee evident in the past few weeks, the withholders far outnumber the reporters. Now the withholders are starting to come clean and soon the H5N1 migration paths will be clear to those who have trouble analyzing data.

The sequences clearly indicated wild birds had been moving flu sequences around forever, but the Qinghai version of H5N1 made it quite obvious to anyone paying attention. Now it is becoming clear even to those not paying attention.

The same thing will happen with recombination. I gave WHO and NIH the data. They have their consultants who have built careers and funding on reassortment. Their two pillars (reassortment and random mutation) are under attack and they will man the barricades at all costs.

However, even those not paying attention can see acquistions (like the China HA cleavage suite missing one R being acquired by Vietnam sequences in northern Vietnam last year).

However, for those paying little attention, there was the prediction that S227N would appear in the Middle East this fall and lead to efficient H5N1 infection of humans. This happened in Turkey and was quite clear. Now its damage control time and S227N is “disappearing” although there were no human cases prior to Turkey and the cluster was easily the largest recorded for H5N1.

WHO will soon be told of the next acquisition. I don’t expect them to do much, but others will know who knew what when, and if the prediction comes true, even those not paying attention will notice, because the effects will be quite clear and the cover-up will be quite difficult.

Stay tuned. The flat earth society days are once again numbered, at least in the area of influenza genetics.

“The flat earth society is alive and well and are still spinning stories to try to explain away S227N, which was quite predictable” -Niman

As demonstrated in my previous post, there seems to be no lack of “spinning” from you. In fact, the WHO can’t hold a candle to the stories you continue to spin.

I’ve asked you many times to prove (ie sequence data) that S227N was in more cases than the lone index in Turkey……….we are waiting. If you are going to accuse, shouldn’t you have the proof to back it up?

Good point Monotreme… But IMO… I wouldn’t exactly go so far as to say that H5N1 is as dangerous as Ebola… I say this because current strain is not as easily transmitted… even by bodily fluids… In other words… get exposed to H5N1 & you might or might not get infected… Get exposed to ebola & you probably will… But I do know that this could change at any time as H5N1 takes more of a liking to mamalian receptors

Niman Haters:

If he’s so full of it, why do most or all of you seem to be reading his website so much?

Niman Haters:

Wouldn’t it be wiser to spend your time reading something else?

anon_22: I created the thread as you suggested.

WildBill: I lay out some of my reasons that H5N1 may be as dangerous as Ebola in a new thread. There are cultural practices unique to Africa which increase the odds of infection. I raise the possibility that when H5N1 meets these customs, it will be amplified just as Ebola or Marburg were. The more time a given strain spends in humans, the better adapted it may become.

maybe I’m missing something, but one single nucleotid/aminoacid beeing replaced by another one (S227N) why should this be recombination ?

I would see it in the 5-acid subsequence included in the NS1-gene making NS1s of lengths 225 or 230. But not when single letters are swapped.

Does anyone know (Henry?) if the gene mutation CCR5-delta 32 could be protective against the cytokine storm??

http://www.abc.net.au/science/features/blackdeath/default.htm

“ In 1996, researchers from the National Institutes of Health in Washington D.C. led by Dr Stephen J O’Brien, tracked down the modern day descendents of Eyam from parish records and tested their DNA. They were curious to know whether the survivors shared any genetic similarity that had helped their ancestors resist the plague. They found high levels of a gene mutation called CCR5-delta 32 amongst the descendents. CCR5 is a gene that codes for a protein on the surface of white blood cells WHICH ACTS AS A RECEPTOR FOR OTHER MOLECULES INVOLVED IN INFLAMATION.

These researchers knew about this protein from previous research on HIV which showed that HIV can slip past the protein, using it as a gateway to get inside and kill white cells. But people who have the mutated form of the gene - CCR5-delta 32 - don’t have this protein and their white cells won’t allow HIV in. So people with the mutation are resistant to HIV infection - they either don’t get HIV at all or are much slower to get it than people who have the normal gene.

Here was the mutation showing up again in the population of Eyam. And not just Eyam. Areas of Europe that had been affected by the plague (including America, which was mostly settled by European plague survivors and their descendents) also had unusually high levels of CCR5-delta 32 - about fourteen per cent of the population compared to two percent in areas that never experienced the Black Death - such as Asia and Africa.

The big jump in the percentage of the population with the mutation has been calculated to have occurred around 700 years ago - around the time of the first major plague epidemic, say Duncan and Scott.

It appears that, beginning 700 years ago, the Black Death increased the genetic frequency of CCR5-delta 32 mutation in the Caucasian gene pool. This protected these populations from later epidemics of both the Black Death and also HIV. The populations of Asia, and Africa had no such protection - and this also explains why HIV/AIDS has spread more quickly there. It also appears that, like HIV, the Black Death was caused by a virus, say Duncan and Scott.”

The data for S227N has been presented and it is the human clusters in Turkey and Iraq. As has been cited many times in the past and confirmed again in Nigeria, the H5N1 being transmitted and transported by wild birds. H5N1 in Russia, Kazakhstan, Mongolia, Romania, Croatia, Ukraine, Greece, Italy, Bulgaria, Slovania, Azerbaijan, Turkey, and Iraq are all the Qinghai strain.

There were no confirmed human cases involving the Qinghai strain until Turkey. The index case had S227N, as predicted. S227N is known to increase the affinity for human receptors. The index case in Turkey initiated a huge familial cluster that involved the hospitalization of at least 16 family members and possibly 24 family members. Included in the hospitalized cases were 7 H5n1 confirmed cases, including all four reported H5n1 fatalities in Turkey. It is quite clear that this cluster was linked to S227N. Now there are similar large clusters in Iraq in the north and south.

The large clusters signal S227N and the signal is quite clear.

The single nucleotide changes are not random mutations. The are quite predictable based on recombination rules as predicted for S227N

http://www.recombinomics.com/News/10220501/H5N1_H9N2_Recombination.html

Clue: To understand what I just said, you actually have to read the comments in the above link as well as embedded links in the commentary.

Flu changes all of the time by single nucleotide changes, which come from recombination, NOT random mutations.

The concept falls under the category of paradigm shift

http://www.recombinomics.com/paradigm_shift.html

is this also the mainstream opinion ?

“The data for S227N has been presented and it is the human clusters in Turkey and Iraq.”

Quit spinning and show the proof Henry.

By the way, is the pandemic still at stage 6?

While Y’all fight it out I’m gonna buy another 50 pounds of rice. Good Luck! =:>

Birds might bring the S227N to North America …

If Dr. Niman is correct about S227N, and Dr. David Nabarro’s comments in this 2/13 article are correct:

Dr David Nabarro, the United Nations bird flu chief, said that the arrival of the virus in Nigeria increased the prospect of it spreading worldwide, because several migratory routes intersect in that country.

Dr Nabarro said: “If it turns out that H5N1 was carried to west Africa by migratory birds, we need to be prepared for the possibility that within the next six months it could be brought back to the northern hemisphere - but perhaps along a different flight route.

“And that could mean that countries in Western Europe and North America should be bracing themselves for the possible introduction of H5N1 avian influenza,” he said.

then migratory birds could bring S227N to North America. Click on the image to see the bird migration paths. This brings the scariness a little too close to home. But then people vectors on airlines might bring it home even earlier.

-keith

Keith, per your map, why do the “Districts with outbreaks” not match the migration paths?

Tram: i didn’t make the make. You’ll have to ask the author of the 2/13 article linked to above. Sorry, I’m just the messenger.

-keith

If you don’t understand it, how can you use it to illustrate your point: “then migratory birds could bring S227N to North America”?

Here is the data on S227N.

WHO/Weybridge has NOT released ANY sequences from Turkey.

S227N is in the receptor binding domain and it increases the affinity for human receptors and decreases the affinity for avian receptors.

Media reports (many including Nature) indicated S227N had been found in the index case, but it was a mixture of S227N plus wild type.

http://www.recombinomics.com/News/01190601/H5N1_Turkey_S227N_E627K.html

Reports also indicated that both chicken eggs and MDCK cells were being used to isolate the H5N1. Initial data came from the index case, but much of the data for most of the genes came from a sister of the index case and that sequence did not have S227N.

The cluster linked to the index case was very large involving three families, 16 hospitalized patients, 7 H5N1 positive including all 4 fatalities with at least 2 H5N1 positive cases from each of the three families. Members of two otehr families, at least one that was definitelt related accounted for 8 more hospitalizations, although none of the eight were confirmed.

http://www.recombinomics.com/News/01220601/H5N1_Kocyigit_Ozcan_Timeline.html

Prior to this cluster, there were no H5N1 human cases linked to the Qingahi strain. After this cluster were additional smaller clusters in Turkey and more recently two large clusters in Iraq.

The interpretation of the above data is that S227N led to the efficient human infections and large clusters. The clusters in Iraq indicate S227N is not limited to the index case in Turkey, but has been transported down to northern and southern Iraq.

Most of the initial sequence data came from the sister because the H5N1 grew well in chicken eggs, eliminating or reducing S227N.

It is well know that growth of flu in eggs selects against polymorphisms that favor mammalial receptors and replaces them with polymorphisms that favor avian receptors.

Thus, the human infections, especially those taht involve clusters, are caused by H5N1 with S227N.

The storied quoting Michael Perdue indicating that S227N was only found in the index case has yet to be published, suggesting that the story was pulled, or at least the quote on the “mutation” was pulled.

Tram, At this stage the migratory bird movement of H5N1 is pretty much a done deal. It was obvious as soon as the Chany Lake sequence data was announced in August of 2005. That should have killed the dead birds don’t fly nonsense, but it was kept alive by wildlife groups and commentaries on Promed (“dead birds don’t fly” and “wild birds as victims”).

However, when the sequences in Nigeria were announced and the were virtually identical to Turkey, Croatia, Ukraine, Romania, Russia, Mongolia, Qinghai, even the holdouts through in the towel,

http://www.recombinomics.com/News/02110601/H5N1_S227N_Transport.html

and now the missing links like Azerbaijan, Iraq and the later responders in Europe like Bulgaria, Greece, Italy, Slovenia have spilled the beans and admitted they too have the same H5N1 as everyone else it is clear that the gaps in the migratory path are due to an absence of reports and not an ansence of H5N1.

If you haven’t got that by now, you shou,d try another topic, because you will never quite understand what is going on with avian influenza in general, and pandemic H5N1 in particular.

gs, The paradigm shift is still shifting. When I showed NIH all of the examples of recombination, they asked why the flu geneticists didn’t believe it. I told them to ask the non-believers.

Flu actually provides some of the strongest data because the database of sequences is large. Those generating and publishing the sequneces are firmly committed to reassortment and random mutation explanations of flu eveolution, which is why they get so many things wrong and think the evolution of H5N1 can’t be predicted.

They are still doing damage control on S227N, but they will almost have to throw in the towel if the next one also comes to pass, so their days are numbered and they will be drowning with data by the spring.

I note that Henry quotes and links only to himself.

Henry, have you read Maria Cheng’s new paper on the stability in the flu genome? It was presented at the APHA conference last month. You weren’t there? You don’t go to conferences or present papers in juried publications? You really should read this one, it pretty much demolishes all of your editorial nonsense.

Henry doesn’t publish and doesn’t go to conferences. To some of you that makes him a maverick scientist. To me, that makes him a coward unwilling to defend his theses. By the way, where is all that science of his? It isn’t published or on his website anywhere.

the Niman-post to NIH, is it available ? Despite that he thinks “their days are numbered”, apparantly it’s still the mainstrain which doubts recombination although Niman always states it as if it were proved. I can’t follow the arguments yet, would have to spend some hours with reading probably… Just doesn’t make sense on first view, when you have _few_ subsequences of length >2 replaced and _lots_ of single nucleotides, that both should be recombination.

When Henry actually posts the studies and science, well, I suspect we’ll all be enjoying another world.

gs, don’t get your hopes up.

Melanie: do you mean because Dr Niman is younger than you or because H5N1 will kill you before you see Niman’s papers if any would be plubished a day?

In general, I agree with Melanie, a valued scientist has to plubish its works to be recognized and that is his main objective share his found to the scientist community… Without any paper published you don’t exist in the scientist community. See the thesis approach to get a doctorat.

Anon_06,

I don’t think the system is perfect, but the publish/critique cycle isn’t a bad one. Henry doesn’t publish or even let his data get out on the Net.

I have no idea if Henry is younger than me, and I don’t see how that matters. Here, we stive for transparency. We aren’t perfect but we are trying. Henry isn’t.

anon6 thought : “another world” = heaven I think: get one’s hope up = keep hoping (?)

gs: yes exactly I thought that Melanie was talking about heaven…

Tram – at 01:07

“Keith, per your map, why do the “Districts with outbreaks” not match the migration paths?”

Let me take a shot.

The map Keith posted (how does he do that, btw?) shows three transcontinental flyways. It also shows many, if not all, HPAI outbreak areas (red dots). The three “empty” flyways are “conduits” to Europe and North America. Other transcontinental flyways overlie the outbreak areas but I think those flyways have been removed for clarity’s sake…to emphasize the conduits to Europe and North America.

Regarding the magic of paying attention, niman recently replied to a flyways question saying the virus is being spread by long range migratory birds (something like that). That isn’t a new theory, and I think by now it’s pretty much taken for granted. The significance of stating explicitly that the spread is mainly due to long range migratory birds must have to do with particular species and their migratory roundtrips.

We have ravens here and they stay in place, don’t go anywhere so far as I can tell. On the other hand, I’m told arctic terns migrate 20,000 miles.

Maybe so.

Anyway, it’s pretty clear that all migratory birds don’t cycle the full extent of their respective transcontinental flyways. A few might, but most would have more circumscribed range. How does that affect spread? You’re the virus; think of the difference between a 5-hop itenary from Miami to Seattle or a direct flight. The more a transcontinental flyway is actually an overlay of many shorter migration paths, the longer it might take you to go from A to B.

Perdue bugs Niman re S227N but he may also bug him re carrier birds. Perdue says there are only a few species carring the virus. If you look at the NIH Flu Database, you’ll find that a fair number of bird species have carried H5N1. Absent more clarity to that comment, I can’t can’t make out if the NIH H5N1 bird species are few by comparison to all avian species, or if Perdue is speaking only of long-range migratory birds. The data I could find aren’t always that specific (“ducks”, for example, or “shorebirds”).

I’m not an ornithologist / virologist, but if what niman says about wild birds is true (and common sense indicates it must be), then it should be possible to formulate some probabilistic infection spreads based on where the virus is endemic now and where the birds might take it next and then next and then next. That kind of estimation might produce an itenary not only lucid, but well described.

S227N : I get : TLNQRLVPK or TLNQRLVPR starting at position 220. What am I missing ? migratory birds: maybe they consider different species more interesting, so the database is biased towards many species. When there are only so few main migration paths EU-Afr,EU-asia,NAm.-SAm, then, couldn’t we stop them from crossing continents, if we wanted to ? (yes, I know there are ecological problems to consider too)

You go Melanie. I couldn’t agree more.

 chillindame,

We work with what we’ve got. Henry isn’t helping.

Counting clues. There are several systems for numbering. Most H5 sequneces will have the S227N at position 238.

As far as the “party line” on how flu evolves goes, I am well aware of drifts and shifts by random mutation and reassortment. Its a good story, but leaves out the main maechanism of influenza evolution, which is homologous recombination.

I have given many examples in a PCT that was filed in June, 2005. Usually, such filings are available to the public, but the US government put a security hold on the patent. The hold has since been lifted, but it remains unclear when the patent will be avilable to the public. That application has lots of pictures (about 100 pages worth) and examples of recombination in H5N1 (which is probably one of the reasons the security hold was placed on the patent application by the US government).

Sooner or later it will be here

http://www.wipo.int/pctdb/en/search-adv.jsp

(you can search NIMAN to get older filings)

Henry,

That link takes one to a blank filing site, not helpful. I still wait for you to have better data than Maria Cheng’s paper at the APHA. If you haven’t read the paper, I have a copy.

I will be putting up a commentary on receptor binding domain, although it is somewhat interesting to watch posters comment on the “two mutations” or S227N with some authority, yet don’t know where the domain is or how to find the avian or mammalian polymorphisms.

Here is one more clue

D190D, G225D, Q226L, S227N, G228S.

As far as most of the scientific world looking at the pandemic is concerned, the above positions are key, but WHO has no idea of when or if they will change.

However, the story is in the sequneces and the H5N1 Qinghai Express is on track and hunting for new acquisitions (and another has already been targetted).

Some with a little scientific background can figure out some of the story form the above clues.

Others just launch personal attacks, which is quite remarkable when the stone throwers don’t appear to have a clue about recombination or how to find data from links posted.

Henry,

And finding any of the scientific data from your site would be making stone soup.

Here is another clue

http://www.recombinomics.com/News/10220501/H5N1_H9N2_Recombination.html

(but you have to actually go to the link and read what is said and look at the donors in the Middle East to understand the earlier prediction).

Melanie, The link is to a seach engine for the filing site. If you type in NIMAN in the seach box, the prior filings will appear and if you click on the filing, you can read the full text of the patent (you should find 3).

If the above is too difficult, you can go to the Recombinomics site

http://www.recombinomics.com/patents.html

If you click on the blue underlined patent number, you can read older US patents that have issued.

If you can’t find the blue underline, here is the beginning of one of the patents (which even has SEQUENCES!)

United States Patent 6,551,789 Niman April 22, 2003

Process for characterizing a biological sample using patterns of oncogene expression

Abstract A method of characterizing a biological sample is provided. The method includes the steps of contacting the sample with at least two receptor molecules to generate a first pattern of reactivity and comparing that pattern to a second reactivity pattern generated by a known sample and indicative of oncogene expression.

Inventors: Niman; Henry L. (Carlsbad, CA) Assignee: The Scripps Research Institute (La Jolla, CA) Appl. No.: 427576 Filed: October 26, 1999

Current U.S. Class: 435/7.23; 435/7.1; 435/7.8; 435/7.92; 435/7.94; 435/7.95; 436/514; 530/388.8; 530/388.85 Intern’l Class: G01N 033/574 Field of Search: 435/7.1,7.8,7.92,7.94,7.95,7.23 436/514 530/388.8,388.85

References Cited [Referenced By]

U.S. Patent Documents 4579827 Apr., 1986 Sakamoto et al. 4699877 Oct., 1987 Cline et al. Foreign Patent Documents 0181635 May., 1986 EP. 0206065 Dec., 1986 EP. 0214520 Mar., 1987 EP. 0221561 May., 1987 EP. 850807 Feb., 1985 WO.

Other References MacLean et al, “Antigenic Heterogeneity of Human Colorectal Cancer Cells Lines Analyzed by a Panel of Monoclonal Antibodies. I. Heterogeneous Expression of Ia-Like and HLA-Like Antigenic Determinants”, Journal of the National Cancer Institute, vol. 69, No. 2 (Aug. 1982), pp. 357–64. RC261.A1U5.* Clark, et al., PNAS-USA 82:5280–5284 (1985). Towbin, et al., PNAS-USA 76:4350–4354 (1979). Niman. et al., PNAS-USA 80:4949–4953 (1983). Hunter, T., Readings from Scientific American: Cancer Biology, W.H. Freeman & Co. NY, pp. 88–97 (1986). Weinberg, R., Readings from Scientific American: Cancer Biology, W.H. Freeman & Co., pp. 77–87 (1986). Bishop, J. Michael, Readings from Scientific American: Cancer Biology, W.H. Freeman & Co., NY, pp. 66–76 (1986). Sen, et al., PNAS-USA 80:1246–1250 (1980). Wong, et al., PNAS-USA 78:7412–7416 (1981). Papkoff, et al., Cell 27:109–119 (1981). Bizub, et al. Oncogene 1:131–143 (1987). Shen, et al., Oncogene 1:157–165 (1987). Srivastava, et al., PNAS-USA 82:38–42 (1985). Niman, et al., PNAS-USA 82:7924–7928 (1985). Niman, J. Clin. Lab. Analysis 1:28–41 (1987). Chesa, et al., PNAS-USA 84:3234–3238 (1987). Young, et al., Immunol. Comm. 11 (1):9–16 (1982). Schmitz, et al., Mol. Immunol. 19:1699–1702 (1982). Sutcliffe, et al., Science 219:660–666 (1983). Shea, et al., Oncogene 1:157–165 (1987). Wilson, et al., Cell 37:767–778 (1984). Bizub, et al. Oncogene 1:131–142 (1987). Niman, et al., PNAS-USA 82:7924–7928 (Dec. 1985).

Primary Examiner: Stucker; Jeffrey Attorney, Agent or Firm: Northrup; Thomas E., Fitting; Thomas

Goverment Interests

This invention was made with government support under Contract Nos. N01-CP-41009, CA 38160 and CA 25803 by the National Institutes of Health. The government has certain rights in the invention.

Parent Case Text

CROSS REFERENCE TO RELATED APPLICATION

Continuation of application Ser. No. 08/461,583, Jun. 2, 1995, U.S. Pat. No. 5,972,629 which is a continuation of application Ser. No. 08/294,879, Aug. 23, 1994, U.S. Pat. No. 5,591,587, which is a continuation of application Ser. No. 08/054,864, Apr. 28, 1993, abandoned, which is a continuation of application Ser. No. 07/900,502, Jun. 16, 1992, abandoned, which is a continuation of application Ser. No. 07/780,415, Oct. 22, 1991, abandoned, which is a continuation of application Ser. No. 07/118,823, Nov. 9, 1987, abandoned, which is a continuation-in-part of application Ser. No. 07/039,534 filed on Apr. 16, 1987, now U.S. Pat. No. 5,015,571, which is a continuation-in-part of application Ser. No. 06/736,545 filed on May 21, 1985, now abandoned, which is a continuation in part of application Ser. No. 06/701,954 filed Feb. 15, 1995, now U.S. Pat. No. 5,030,565, which is a continuation in part of PCT application PCT/US84/01304 filed Aug. 17, 1984 wherein the U.S. National Phase was entered on Feb. 15, 1985 Ser. No. 06/713,410, now abandoned, which is a continuation-in-part application of U.S. application Ser. No. 06/524,084, filed Aug. 17, 1983, now abandoned.

Claims

I claim:

1. A method of characterizing a biological sample comprising:

(a) contacting a biological sample with at least two different receptor molecules to generate a first pattern of reactivity; and,

(b) comparing said first pattern of reactivity to a second pattern of reactivity generated by a known biological sample wherein said second pattern is indicative of expression of oncogene or oncogene-related sequences.

Description

TECHNICAL FIELD

The present invention relates to immunological receptors and ligands, and more particularly to monoclonal receptors raised to polypeptides who whose amino acid residue sequences correspond to sequences of retroviral oncoprotein ligands.

BACKGROUND ART

Retroviruses are viruses that contain a single strand of RNA as the genetic material rather than DNA. The single-stranded RNA genome of each of these viruses gives rise to a double-stranded DNA molecule after the virus infects a susceptible host. This DNA replica of the viral genome then introduces itself permanently into a chromosome of the successfully infected cell and replicates in that host chromosome.

The retroviruses discussed hereinafter and in the claims may be further defined as being replication-defective retro-viruses. Thus, these viruses do not themselves contain a gene encoding the reverse transcriptase usually required to permit the viral RNA genome to be translated into a DNA that can be introduced into a chromosome of the infected host. Rather, the retro-viruses discussed hereinafter typically must be complimented in their infection by a so-called helper virus that is replication-competent. That second virus contains the gene that encodes the reverse transcriptase enzyme that incorporates the genomic materials from both viruses into the successfully infected host cells to transform those cells.

For ease in understanding, the replication-defective retroviruses will be discussed hereinafter and in the claims merely as retroviruses with the understanding that they are replication-defective and require the assistance of a helper virus for successful infection and transformation of host cells. This usage of the term retrovirus is known in the art and has been used in the art as such without further explanation.

Some members of the retrovirus family are highly oncogenic as judged by their ability to cause the formation of solid tumors within a short period of time after being inoculated into the host. These viruses can also cause “cancerous” changes in cells grown and cultured in the laboratory; such changes are called “transformations” and provide a reliable in vitro biological assay for oncogenic viruses. Several such viruses have been isolated from chickens, turkeys, mice, rats, cats and monkeys.

A single gene, the oncogene, located on the genome of these highly oncogenic viruses is responsible for the tumorgenic potential of the virus. In the case of several viruses, the protein products of their oncogenes, referred to herein as oncoproteins, have been immunologically identified by taking advantage of the fact that serum from an animal bearing a virus-induced tumor contains antibodies directed against those oncoproteins.

A rapidly growing body of evidence indicates that the oncogenes of retroviruses are closely related to and are derived from specific genetic loci in the normal cellular genetic information of all vertebrates.

Interest in oncogenes has steadily risen in the last decade. Although RNA tumor viruses have been implicated as the causative agents of experimentally induced neoplasia in chickens for over 50 years, it was not until the mid 1970s that mechanisms of virally induced neoplasia began to emerge [Bishop (1983) Ann. Rev. Biochem. 52:301–54]. According to one such mechanism, replication-competent avian viruses and defective mammalian viruses had captured cellular genes that provided the viruses with a transforming potential.

Molecular hybridization studies using specific nucleic acid probes, followed by genetic cloning of viral oncogenes and their cellular relatives by recombinant DNA technology, have established the kinship between retroviral oncogenes (v-onc) and cellular oncogenes (c-onc) found in all normal vertebrate cells. Molecular analysis of the several retroviruses thus far isolated has revealed more than two dozen different oncogenes. In most cases, a corresponding cellular to the retroviral oncogene or oncoprotein has been isolated.

For example, the human EJ or T24 bladder carcinoma oncogene was identified as the homolog of the transforming gene of Harvey murine sarcoma virus (ras.sup.Ha) and also of the BALB sarcoma virus (bas) [Parada et al., Nature, 297, 474–478 (1982); Der et al., Proc. Natl. Acad. Sci USA, 79, 3627–3634 (1982); and Santos et al., Nature, 298, 343–347 (1982)]. In addition, the oncogene of the human carcinoma cell line LX-1 was found to be homologous to the transforming gene of Kirsten strain of murine sarcoma virus (ras.sup.Ki) [Der et al., above]. Still further, the v-onc for a c-onc designated fps of avian origin is represented at least twice among a limited number of avian retrovirus isolates; its mammalian cognate designated fes in feline species is found in two different strains of feline sarcoma viruses.

The homology [Doolittle et al., (1983) Science 221:275–277; Waterfield et al., (1983) Nature 304:35–39] between the gene product of the sis oncogene and one of the chains of platelet-derived growth factor provided the most solid link between malignant transformation by oncogenes and stimulation of normal cell division by growth factors. This identity between oncogene products and growth factors and cellular receptors was further substantiated with sequence analysis of the epidermal growth factor cellular receptor [Downward et al., (1984) Nature 307, 521–527; Ullrich et al., (1984) Nature 309:418–425] that was found to be the normal homologue of erb B. Furthermore, immunological cross-reactivity of fms antibodies with colony stimulating factor-1 receptor [Sherr et al., (1985) Cell:665–676] as well as protein kinase homology with the insulin-receptor [Ullrich et al., (1985) Nature:313, 756–761] and platelet derived growth factor receptor [Yarden et al., (1986) Nature 323; 226–232] indicated the kinase activity of many of the sequenced oncogenes would be important in the signal transduction of several growth factors.

Sequencing of oncogenes captured by retroviruses or identified via transfection experiments greatly extended the number of kinase family members. [Hunter et al., (1985) Ann. Rev. Biochem. 54:897–930.] This sequence analysis suggested the number of kinase-related proteins would be large and the family members could be divided into subgroups based upon sequence homology and overall structural similarities. The kinase family can be conveniently divided into gene products that do or do not have extracellular (hormone/growth factor) binding domains.

The close similarity between the kinase portion of src and yes has been apparent for several years. [Kitamura et al., (1982) Nature 297:205–208.] Recently, sequencing of additional genes has extended this homology to fgr, [Naharro et al., (1984) Science 222;63–66] lck, [Marth et al., (1985) Cell 43:393–404. syn, [Semba et al., (1986) Proc. Natl. Acad. Sci. USA 83:5459–5463] and lyn [Yamanashi et al., (1987) Mol. and Cell Biol. 1:237–243]. All six of these genes encode proteins of approximately the same size 55–65 kd, and the genes share intron/exon borders indicating they evolved from the same ancestral proto-oncogene. However, each gene is located on a separate chromosome and expresses different proteins in different tissues.

Many additional kinase family members can also be placed into subgroups. Mos [Van Beveran et al., (1981) Nature 289:258–262] is closely related to pim-1 [Selten et al., (1986) Cell 46:603–611], one of the preferred integration sites of Moloney leukemia virus. Abl [Reddy et al., (1983) Proc. Natl. Acad. Sci. USA 80:3623–3627] is closely related to arg [Kruh et al., (1986) Science 234:1545–1547]. Fes [Hampe et al., (1982) Cell 30:775–785] and fps [Shibuya et al., (1982) Cell 30:787–795]. represent the mammalian and avian counterparts of the same gene.

Similarly, raf [Sutrave et al., (1984) Nature 309:85–88] and mil [Mark et al., (1984) Science 224:285–289] are mammalian and avian homologues of the same gene. They are closely related to A-raf/pks [Huleihel et al., (1986) Mol. and Cell Biol. 6:2655–2662; Mark et al., (1986) Proc. Natl. Acad. Sci. USA 83:6312–6316].

A subgroup that does not have a viral counterpart contains genes that encode protein kinase C, the receptor for phorbal esters. There are at least three closely related genes comprising this subgroup [(Coussens et al., (1986) Science 233:859–866; Knopf et al., (1986) Cell 46:491–502]. Moreover, one of the genes can encode two proteins via alternative exon usage [Ohno et al., (1987) Nature 325:161–166]. Other more distantly related cytoplasmic kinases include cAMP- and cGMP-dependent protein kinase [(Shoji et al., (1981) Proc. Natl. Acad. Sci USA 78:848–851; Takio et al., (1984) Biochemistry 23:4207–4218], as well as myosin light chain kinase [Takio et al., (1985) Biochemistry 24:6028–6037]. Several transmembrane kinases have also been sequenced in the past few years.

A gene closely related to the human epidermal growth factor receptor (HER) has also been found in humans (HER-2) [Coussens et al. (1985) Science 230:1132–1139] and rats (neu) [Bargmann et al., (1986) Nature 319:226–230]. The growth factor that binds to ros [Neckameyer et al., (1985) J Virol. 53:879–884] is not known although the sequence is most closely related to the insulin receptor (HIR) [Ullrich et al., (1985) Nature:313, 756–761]. The colony stimulating factor 1 receptor, FMS [Hampe et al., (1984) Proc. Natl. Acad. Sci. USA 81:85–89], forms a sub-group with kit [Besmer et al., (1986) Nature 320:415–421] and the receptor for platelet-derived growth factor, PDGF-R [Yarden et al., (1986) Nature 323:226–232]. In addition, sequences for the trk [Martin-Zanca et al., (1986) Nature 319:743–7481 and met-8 [Dean et al., (1985) Nature 318:385] oncogenese have been published, although the corresponding growth factors are not known.

A similar although not as extensive expansion has also been seen for the nucleotide binding proteins represented by the ras oncogene family. Sequence data indicate bas [Reddy et al., (1985) J. Virol. 53:984–9871 is the mouse form of H-ras [Dhar et al., (1982) Science 217:934–937], and that the H- and K-ras products differ principally at the carboxyl region [Tsuchida et al., (1982) Science 217:937–939]. Through alternative exons K-ras can encode 2 proteins (4A and 4B) [McGrath et al., (1983) Nature 310:501–506]. A third member, N-ras, also diverges from H- and K-ras in this region [Taparowsky et al., (1983) Cell 34:581–586]. Another closely related gene is R-ras [Lowe et al., (1987) Cell 48:137–146], although this gene is closely related to the three ras genes that have evolved from the same ancestral gene, R-ras has different intron/exon boarder. Another gene, rho [Madule et al., (1985) Cell 41:31–40], has scattered regions of homology with ras. Furthermore, a third group, ral, also has similar regions of homology [Chardin et al., (1986) EMBO J. 5:2203–2208]. Moreover, a yeast gene ypt [Gallwitz et al., (1983) Nature 306:704–707] has regions of homology with ras and this gene is distinct from the two yeast genes that have extensive homology with ras; i.e., they are more like R-RAS.

Other genes that also have homology with ras include the G proteins [Itoh et al., (1986) Proc. Natl. Acad. Sci. USA 83:3776–3780] as well as transducin and elongation factor, Tu [Lochrie et al., (1985) Science 228:96–99]. The G proteins are composed of subunits that stimulate (G.sub.s) and inhibit (G.sub.i) adenylate cyclase. Another related protein (G.sub.o), has an unknown function. These proteins exists in a variety of different forms that have closely related sequences.

The nuclear proteins myb [Rushlow et al., (1982) Science 216, 1421–14231, myc [Colby et al., (1983) Nature 301:722–725] and fos [van Straaten et al., (1983) Proc. Natl. Acad. Sci. USA 80:3183–3187] comprise another family of oncogenes that are related more by cellular location than sequence. However, additional genes related to these oncogenes have been identified. N-myc [Stanton (1986) Proc. Natl. Acad. Sci. USA 83:1772–1776] and L-myc [Nau et al., (1985) Nature 318:69–73] sequences have been published, and unpublished related sequences have been identified. Moreover, the sequences are distantly related to fos. A related fos (r-fos) [Cochran et al., (1984) Science 226:1080–1082] sequence has been published, and unpublished data indicate a phosphorylase inhibitor has limited homology as does the jun oncogene.

Another group of nuclear oncogene-related proteins include steroid and thyroid hormone receptors. Although only one sequence related to erb A has been published [Sap et al., (1986) Nature 324:635–640; Weinberger et al., (1986) Nature 324:641–646], hybridization studies indicate at least two related sequences are present in the human genome (Weinberger et al., (1986) Nature 324:641–646]. Steroid receptor sequences indicate erb A (the thyroid hormone receptor) is part of a superfamily that includes several receptors (estrogen, glucocorticoid, progesterone, aldosterone) [Greene et al., (1986) Science 231:1150–1153; Rollenberg et al., (1985) Nature 318:635–641; and Connelly et al., (1986) Science 233:767–770].

In the growth factor group only the PDGF-1 chain [Doolittle et al., (1983) Science 221:275–277 and Waterfield et al., (1983) Nature 304:35–39] has sequence homology to sis (PDGF-2). However, other growth factors [Gregory (1975) Nature 257:325–327; Marguardt et al., (1983) Proc. Natl. Acad. Sci. USA 80: 4684–4688] (EGF and TGF) bind to the product of the erb B protooncogene, and CSF-1 [Kawasaki et al., (1985) Science 230:291–296] binds to the fms protooncogene. Moreover, TGF [Derynk et al., (1985) Nature 316:701–705], forms another subgroup by virtue of homologies with Mullerian inhibitory substance [Cate et al., (1986) Cell 45:685–698], and the three chains that are found in the various forms of inhibitin [Mason et al., (1985) Nature 318:659–663 and Vale et al., (1986) Nature 321:776–779].

Finally, sequences representing two of the preferred integration sites of MMTV have been published [Van Ooyen et al., (1984) Cell 39:233–240 and Moore et al., (1986) EMBO J. 5:919–924].

Thus, in the past few years, the number of related published sequences has increased dramatically. These sequences suggest that a limited number of pathways controlling cell division and differentiation exist but that many different members may participate in this control.

An example of transduction of only a portion of a cellular gene by a retrovirus is the erb B oncogene. The erb B oncogene is highly homologous to a portion of the ECG receptor [Ullrich et al., Nature 309:418 (1984)], as already noted. Sequence analysis of the entire receptor gene demonstrates the relatedness of erb B with the entire intracellular domain, the transmembrane domain, and a portion of the extracellular doman.

The protein encoded by the viral oncogene and the corresponding, homologous protein within the host cell are both referred to herein as oncoproteins, although the cellular oncoprotein is typically larger and is present in small quantities in normal cells, and thus need not only be associated with neoplastic states. In addition, oncoproteins encoded by related oncogenes can have different molecular weights, e.g., the p85 and p108 oncoproteins encoded by v-fes.sup.ST and v-fes.sup.GA, respectively, and the 100–105 kilodalton (also kd or K dalton) protein of normal mink cells thought to be encoded by the c-fes gene. [Sen et al., Proc. Natl Acad. Sci. USA, 80, 1246–1250 (1983).] The term oncoprotein is thus used generally herein for proteins whose genes and amino acid residue sequences are homologous, at least in part, as discussed hereinafter.

The oncoprotein is generally not present in the virus particle that infects the cell, but is only expressed after infection and transformation. The corresponding cellular oncoprotein is expressed at most minimally in normal cells and to a greater extent in neoplastic cells. Thus, the oncoprotein cannot typically be obtained from the virus. In addition, isolation of oncoproteins from cells is made difficult because of small amount present, the complex mixture of proteins found in normal cells, and the relatively small amount of such proteins present even in transformed cells.

Oncoproteins encoded by v-onc and c-onc genes thus typically contain large sequences of amino acid residues that are homologous, but nevertheless are not usually identical. In addition, oncoproteins encoded by genes of different viral strains, each of which contains ostensibly the same oncogene, have been found to have slight variations in their amino acid residue sequences as exemplified above, and by the four published sequences of the ras gene which differ at the position of the twelfth amino acid residue. Thus, even when oncoproteins are in hand, it may be difficult to distinguish among them.

Immunologically induced receptor molecules such as monoclonal and polyclonal antibodies or the idiotype-containing portions of those antibodies are useful in purifying protein ligands to which they bind, as diagnostic reagents for assaying the presence and quantity of the protein ligands, as well as for distinguishing among homologous protein ligands.

The difficulties associated with obtaining quantities of oncoproteins typically militate against the preparation of receptors to those oncoproteins, although whole cell-induced monoclonal antibodies to v-fes and v-fps encoded oncoprotein have been reported by Veronese et al., J. Virol., 43, 896–904 (1982). In addition, even were whole proteins available for use as immunogens for inducing the production of such receptors, the use of large protein molecules as immunogens produces antisera containing polyclonal antibodies to the numerous epitopes of the large protein molecules.

Hybridoma and monoclonal antibody techniques utilizing whole proteins or large protein fragments as immunogens have been useful in narrowing the immunological response to such immunogens. However, such technology as heretofore practiced has been extremely time consuming and has provided only a relatively small number of hybridomas that secrete useful antibodies that recognize the immunogen. Moreover, even when successful, such techniques cannot be predictive of the chemical identity of epitope to which the receptor molecules are raised. Consequently, even after immunogen-recognizing receptors are produced, the obtaining of receptors to specific, chemically identified epitopic portions of the protein ligand has been a hit or miss operation that still further reduces the number of useful hybridomas that are ultimately produced.

Arnheiter et al., Nature, 294, 278–280 (1981) reported on the production of monoclonal antibodies that were raised to a polypeptide that contained 56 amino acid residues and corresponded in amino acid residue sequence to the carboxy-terminal portion of an intact interferon molecule. The 56-mer polypeptide thus corresponded to approximately one-third of the sequence of the intact molecule.

Arnheiter et al. reported on the production of eleven monoclonal antibodies. However, only one of those eleven monoclonal antibodies bound both to the polypeptide immunogen and also to the intact interferon molecule. In addition, that binding was not very strong as judged by the 3000-fold excess of intact interferon required to compete the antibody away from the synthetic polypeptide. None of the other monoclonal antibodies bound to the intact molecule.

In addition, the production of the hybridomas secreting those monoclonal antibodies required the spleens from three immunized mice. The low yield of the desired interferon-binding monoclonal antibodies, and the fact that three mouse spleens were needed for the preparation of those hybridoma cell lines indicates that those workers were relatively unsuccessful in their efforts.

Lerner et al. have been successful in obtaining protection of animals by the use of vaccines against pathogens by utilizing synthetic amino acid residue sequences of short to moderate length as immunogens. See Sutcliffe et al., Science, 219, 495–497 (1983).

However, it must be understood that until the present invention, successful preparation of hybridomas and their secreted monoclonal receptors differs from the successful preparation of a vaccine containing oligoclonal receptors. Thus, for a high yield monoclonal antibody preparation, it is necessary to stimulate B-cells to secrete large amounts of avid antibodies. On the other hand, for a synthetic vaccine, a wider spectrum of oligoclonal antibodies may be produced in smaller amounts and with lower avidities. In addition, protection of an animal against a pathogen typically requires both T-cell and B-cell activations so that a cellular response and a humoral response, respectively, can be induced in the animal.

A popular explanation for the success of synthetic polypeptide-containing vaccines in generating antibodies that recognize intact proteins and protect animal hosts involves a stochastic model in which the diversity of the immune response allows the observation of an infrequent event; i.e., the polypeptide adopting the confirmation of its corresponding sequence in the native molecule. The concept that moderate-length polypeptides can frequently conform to native structures is contrary to theoretical and experimental studies. Rather, such polypeptides are thought to exist as an ensemble of a large number of transient conformational states that are in dynamic equilibrium. T-Cell activation by, and B-cell production of antibodies raised to, some of that conformational ensemble have been believed sufficient to provide protection upon vaccination.

BRIEF SUMMARY OF THE INVENTION

The present invention contemplates a monoclonal receptor molecule that binds both (a) to a protein ligand encoded by a retrovirus gene, and (b) to a polypeptide of moderate length, about 7 to about 40 residues, and preferably about 10 to about 30 amino acid residues, having an amino acid residue sequence corresponding to an amino acid residue sequence of a portion of the protein encoded by a gene of a retrovirus. The receptor molecule is raised to (induced by) an immunogen containing the polypeptide. Most preferably, the receptor molecule is a monoclonal receptor of the IgG class of immunoglobulins.

Specific, preferred monoclonal receptor molecules of this invention bind to protein encoded by the oncogenes listed below, and also to the polypeptide(s) listed opposite those oncogenes:

        Oncogene      Polypeptide Sequence
        fes           SDVWSFGILLWETFSLGASPYPNLSNQQTR;
                      SPYPNLSNQQTR;
                      IGRGNFGEVFSG;
                      LMEQCWAYEPGQRPSF; and
                      VPVKWTAPEALNYGR;
        myb           RRKVEQEGYPQESSKAG;
                      RHYTDEDPEKEKRIKELEL; and
                      LGEHHCTPSPPVDHG;
        fos           SGFNADYEASSRC;
                      LSPEEEEKRRIRRERNKMAAAKC; and
                      RKGSSSNEPSSDSLSSPTLL;
        sis           RKIEIVRKKPIFKKATV;
                      RVTIRTVRVRRPPKGKHRKC; and
        ras           YREQIKRVKDSDDVPMVLVGNKC;
                      YTLVREIRQHKLRKLNPPDESGPGC;
                      YTLVREIRQYRLKKISKEEKTPGC;
                      KLVVVGARGVGK;
                      KLVVVGASGVGK; and
                      KLVVVGAGGVGK;
        myc           CDEEENFYQQQQQSEL;
                      PAPSEDIWKKFEL;
                      LPTPPLSPSRRSGLC;
                      CSTSSLYLQDLSAAASEC; and
                      CTSPRSSDTEENVKRRT;
        mos           LPRELSPSVDSR;
                      IIQSCWEARGLQRPSA;
                      LGSGGFGSVYKA;
                      RQASPPHIGGTY; and
                      TTREVPYSGEPQ;
        erb-A         KSFFRRTIQKNLHPTYSC;
                      VDFAKNLPMFSELPCEDQ; and
                      CYGHFTKIITPAITRVVDFA;
        erb-B         ENDTLVRKYADANAVCQ;
                      LGSGAFGTIYKG; and
                      IMVKCWMIDADSRPKF;
        PDGF-2        SLGSLTIAEPAMIAECK;
                      RKIEIVRKKPIFKKATV; and
                      RVTIRTVRVRRPPKGKHRKC;
        PDGF-1        SIEEAVPAECKTR;
        EGF           CLHDGVCMYIEALDKYAC;
        abl           LMRACWQWNPSDRPSF;
                      LGGGQYGEVYEG; and
                      LWEIATYGMSPYPGIDLSQVY;
        fms           FMQACWALEPTRRPTF; and
                      LGTGAFGLVVEA
        src           LMCQCWRKDPEERPTF;
                      LGQGCFGEVWMG; and
                      CGSSKSKPKDPSQRRRS;
        yes           LMKLCWKKDPDERPTC; and
                      LTELVTKGRVPYPGMVNREVL;
        fgr           LTELTTKGRVPYPGMGNGEVL;
        bas           KLVVVGAKGVGK;
        int-1         LHNNEAGRTTVFS;
        mil/raf       LVADCLKKVREERPLF; and
                      IGSGSFGTVYRG;
        ros           LGSGAFGEVYEG;
                      VWETLTLGQQPYPGLSNIEVL; and
                      LMTRCWAQDPHNRPTF.

I agree with Henry Niman that the personal attacks are completely uncalled for. Listing of ‘previous niman errors’ is as invaluable as listing previous niman successes, but personal attacks are unnecessary. The data will stand on its own. Reminders about following Forum rules, including respecting each other, still apply.

I will remind niman that in the ‘Niman Chronicle’ threads he promised us a prediction. I hope it’s soon so we can talk about the science and tha data. And I will remind niman that the Forum rules apply to him as well.

In the meantime, please tone down the rhetoric.

You might note that one of the references in the patent is

Wilson, et al., Cell 37:767–778 (1984). The Wilson is Iam Wilson who was the senior author on the glycan chip paper that is the basis for the “two mutations to a pandmeic comment”.

The cell paper cited abovee is at

The structure of an antigenic determinant in a protein.

and if you can’t click on the above link, here is what the abstract says

The structure of an antigenic determinant in a protein.

Wilson IA, Niman HL, Houghten RA, Cherenson AR, Connolly ML, Lerner RA.

The immunogenic and antigenic determinants of a synthetic peptide and the corresponding antigenic determinants in the parent protein have been elucidated. Four determinants have been defined by reactivity of a large panel of antipeptide monoclonal antibodies with short, overlapping peptides (7–28 amino acids), the immunizing peptide (36 amino acids), and the intact parent protein (the influenza virus hemagglutinin, HA). The majority of the antipeptide antibodies that also react strongly with the intact protein recognize one specific nine amino acid sequence. This immunodominant peptide determinant is located in the subunit interface in the HA trimeric structure. The relative inaccessibility of this site implies that antibody binding to the protein is to a more unfolded HA conformation. This antigenic determinant differs from those previously described for the hemagglutinin and clearly demonstrates the ability of synthetic peptides to generate antibodies that interact with regions of the protein not immunogenic or generally accessible when the protein is the immunogen.

MeSH Terms: Amino Acid Sequence Antibodies, Monoclonal/immunology Antibodies, Viral/immunology Antibody Specificity Epitopes* Hemagglutinins, Viral/immunology* Influenza A virus/immunology Models, Molecular Oligopeptides/immunology Protein Conformation Research Support, U.S. Gov’t, P.H.S.

Substances: Antibodies, Monoclonal Antibodies, Viral Epitopes Hemagglutinins, Viral Oligopeptides

Grant Support: AI 19499–01/AI/NIAID CA 25803/CA/NCI

PMID: 6204768 [PubMed - indexed for MEDLINE]

I have to say, I am starting to see Melanie’s point. People around the web seem to have lionized Dr. Niman to the point that he can continue to build his reputation by dropping his hints, and speak crytpically, and make hundreds of declarations (re: Tram’s earlier post), and to the extent that he continues to do this without open and focused criticism, is the extent to which the community loses a chance to find the truth faster. In other words, if we just blindly follow Niman’s pronouncements, we might miss what someone else is saying that might in fact be closer to the truth.

Peer review is rarely a pleasant experience, and Dr. Niman may have found a way to avoid it altogether. Perhaps Niman is one of the first of a new breed of “scientist-bloggers”. Now, did he find this strategy by random mutation or recombination? If by recombination, how quickly will we see the occurrence of new cases of scientist-bloggers? The world is watching with baited breath.

Dr. Niman,

It is now “next week”. We watch for your signal, sir. If the WHO won’t or can’t tell us due to secrecy / incompetence, then when will you be at liberty to discuss your proposals.

Do you have any concerns about PF51 occuring due to human travel from / to the Olympics. Are population concentrations in Lagos of concern . . . millions of incubators with weakened immune systems due to multiple pathogen infestation. When do you foresee or do you care to speculate on humans becoming a significant risk vector in incubating the A isolates that will donate negatively to H5N1? Do you believe that the human population will ever reach a stage / percentage of infectivity that will make us a significant contributor mathematically of conserved, pathogenicity-inducing donor segments / nucleotides? Are you studying any other species (outside the usual suspects) as significant to the incubator of donators chain?

take that!

DemfromCT,

I have given simple links that most can follow to get more information. It becomes annoying when those that have trouble clicking on a hyperlink, put up posts indicating that data that is a click away doesn’t exist, especially when such posters run a website on flu!

It is also annoying when the same people complain about the link!

I have pretty much ignored such nonsense, but if you go back through the thread, ignoring the nonsense was interpreted by the posters as licnese to put up more nonsense.

At some point it is necessary to call a clueless post a clueless post (or a long series of clueless posts).

This thread seems to have become a lightning rod for clueless posts, which at some point need to be called.

I agree that personal atacks are pretty useless, although they do shed some light on the posters launching such attacks.

Niman, STart a thread at your website, I for one would follow it.

The patent posted is based on this paper

http://www.pnas.org/cgi/content/abstract/80/16/4949

If you click on the link you can see the abstract pasted below, or the full paper. This paper descibes a series of monoclonal antibodies made against HA peptides (as well as other peptides including those of oncogenes). One of the flu monoclonals has become one of the most popular monoclonals ever made and is used by almost every major molecular biology research facility in the world.

Here is the PNAS abstract:

Generation of Protein-Reactive Antibodies by Short Peptides is an Event of High Frequency: Implications for the Structural Basis of Immune Recognition

Henry L. Niman, Richard A. Houghten, Leslie E. Walker, Ralph A. Reisfeld, Ian A. Wilson, James M. Hogle, and Richard A. Lerner

Recent studies have shown that chemically synthesized small peptides can induce antibodies that often react with intact proteins regardless of their position in the folded molecule. These findings are difficult to explain in view of the experimental and theoretical data which suggest that in the absence of forces provided by the folded protein, small peptides in aqueous solution do not readily adopt stable structures. In order to rationalize the two findings, there has been general acceptance of a stochastic model which suggests that the multiple conformers of a peptide in solution induce sets of antibodies with a small percentage reactive with conformations shared by the folded protein. This stochastic model has become less tenable as the success rate for the generation of protein-reactive anti-peptide antibodies has grown. To test the stochastic model, we have used monoclonal anti-peptide antibodies as a way of estimating the frequency with which small peptides induce antibodies that react with folded proteins. We have made monoclonal antibodies to six chemically synthesized peptides from three proteins. The frequency with which the peptides induce protein-reactive antibodies is at least 4 orders of magnitude greater than expected from previous experimental work and vastly different from what would be predicted by calculating the possible number of peptide conformers in solution. These findings make the stochastic model less likely and lead to consideration of other models. Aside from their practical significance for generation of highly specific reagents, these findings may have important implications for the protein folding problem.

It’s a truly interesting thing, Henry. As a veteran poster and moderator, I have found over the years that many people simply don’t click on and follow links. You’ve likely noticed this, too. Stories and posts that are well researched with background don’t get read the way the auther intended. The internets are not used to their full potential, especially for those with slower machines or hook-ups.

Because of this, it’s helpful to adjust the writing style to include more in the post and use the background links for those who wish to explore. It’s more work for the author, but a better read by everyone else. Just saying, and that applies to everyone… it’s why dropping a link with no commentary or text gets people to yell at the poster…

Next question: do people want this thread to continue or should we close it and wait for Henry Niman to start a new one based on data and/or predictions?

Scientist-bloggers silent!

Is that what you are asking Donnelly? Or possibly not? Scientist-bloggers unite! Is that it? No? Are we all participating voluntarily, gathering info and providing info interactively . . . with a goal to form a well-considered, cohesive plan(s) of action? I lament these times when those volunteering dissenting information are pushed immediately outside the circle. Some of us are still interested in researching outside the circle. Please allow us this opportunity to study Dr. Niman’s synergistic ideas. Please ponder now, there are two sides to every circle. Apparently, some of you are extremely disinterested in any side but the “inside”? Stand on the line and just edge over / around the parallax, look on the other side. See now, you’re undamaged. Rinse / repeat. It can get to be a habit. Consider your own theories developing deeper roots and broader foundations.

Do any of you recall the multiple fraudulent peer-reviewed papers that have been recanted in the past five years? No system is perfect

You can do a simple google search for 12CA5 monolclonal and get ober 43,000 references to the flu monoclonal that is popular (and described in the 1983 PNAS paper)

link

DemFrom CT - New thread PLEASE - just data and (hopefully) predicitions.

Dem,

The link for niman’s google worked before your fix and in your fix you dropped my comment at 07.32. Can you retrieve it?

done, I think.

OK, thanks.Seems to be position 239 then :
(HA,220:)TLNQRLVPKIATRSKVNGQN human/Hong Kong/213/2003
(HA,220:)TLNQRLVPRIATRSKVNGQS human/Thailand/5(KK-494)/2004
Compressed sequence(1):(2)v(6)s(5)st(7)k(8)r(9)s(3)t(1)i(4)
Compressed sequence(2):(2)a(6)n(5)na(7)r(8)k(9)n(3)a(1)t(4)
Positions for the unmatched letters :
102 136 171 172 205 228 _239_ 279 529
I couldn’t find/understand an argument, why this should have evolved by recombination yet.

…”To me, that makes him a coward unwilling to defend his theses.”…

DemFromCT nailed it: …”Forum rules, including respecting each other, still apply.”

Moderators here have threatened several posters with expulsion (and possibly have expelled a few who are now MIA) for less of a verbal attack than demonstrated in the quote listed above.