Forum: Final Adaptation of H 5 N 1 to Humans Role of Mammalian Reservoirs II

It’s a shame the last fine thread is so hard to read, hope it can be fixed.

One more idea regarding P2P and P2H. This virus presumably is ambidextrious; crossing between pig and birds now, with no barrier between the two. It is well adapted to both, which has happened before. That’s not news, pigs get fed chicken manure, pigs get viruses from chickens. In pigs it could pick up mammal advantages and ricochet back through birds. Since pigs don’t fly, the trans-species virus can fly to other farms and infect poultry, pigs/mammals or ‘certain’ people. It is not surprising that only one dead cat has been sequenced in Indonesia, rather it’s surprising ANY dead animal was reported and sequenced. Yes, we really should have much more investigation going on (about different animals), in order to understand how this incredible feat is happening. The point of semantics warping our views has been made before in threads. Watch out with the words -‘positive/adaptive/selection pressure’. It leads to a belief that there has to be a reason for mutations. It looks like reasonable progression only in hindsight I put a higher priority on “design by accident”. We put a value of advantage on it only because it is still around. This is worth hammering about because of the danger-factor difference in the two beliefs- selection and accident. All scientist know the mutations are random, but too much power is given to there being a reason for a change to occur. Some say “there’s no reason for it to change to a human adapted virus, that would be extremely rare,” etc. There never is a reason for a virus to cross species, it just does it. 90% of the viruses being created in a cell are wrong mutations. If one of these mistakes land in the right mistaken spot, it just keeps going. It has no purpose and doesn’t know where it’s going, but in its shotgun method, it gets there. That’s what’s so dangerous to consider: it’s a plain and simple fluke. We aren’t protected by “it’s not suppose to do that.” People like Fauci are misleading the media and public, by saying there is no need for great concern. How can he sweep aside history, and the process that has led to so many human deaths over the centuries as “no need for concern”? And these “calmsayers” say it can just disappear or mutate down to harmlessness. A few humans have been killed before by a virus that flared up and was stamped out. But that was a single location event. This virus is all over and can not be culled out. Another big point, is that in our 60 years of knowing about bird virus types, we have not seen any of them disappear or go extinct. They could change, but this one would have to change simultaneously around the world. As long as it is successfully procreating, it’s not likely to be displaced by a weaker version. When a virus has stumbled upon a winning game, such as polio, small pox, AIDS, it can keep going for decades without mutating down. I do believe that the human mutated version could be different (but not neccessarily hugely different) and that human influenzas do normalize eventually, after being a pandemic. I see H5N1 being so broadcasted and having such a toehold in humans as Very Bad News. Remember that the virus is more prevalent Oct.- March. I see optimism as an emotional preference rather than a sensible one.

Bringing forward the points I agreed with on the previous thread. Hope other recent posters could move their ideas again.

• Monotreme- pig reservoirs allowing mammalian adaptian, many multi factors involved in infectious diseases.
• Racter- more spread through birds mean more people infected,

the virus is “exploring” little pockets of genetic susceptibility in human populations.

• Tom DVM- once the virus randomly leaps, then selecive adaption can occur.

H5N1 is so deeply entrenched in Asia, so endemic, that really, how can a pandemic from it be avoided?

I think we passed the point of no return a while ago.

Hi everyone. Just a point for discussion. I have been struggling with the genetic susceptibilty argument because it seems to obvious to be true.

So we have a virus that has so far infected approx. 250 persons in several countries around the world…right.

OK, if we are going to use the genetic susceptibility argument for the clusters than this virus must have unbelievable and unique ability only to pick out and infect genetically susceptible persons…and even a more select choice mechanism to only infect people whose offspring are genetically susceptible on one side of the family.

Genetic predisposition or susceptibility could explain one large cluster but could not explain the distribution of this disease…it isn’t remotely possible statistically.

A second issue that troubles me is the issue that the virus is attempting to adapt to birds and to other mammals by mistake…so to speak.

If this was the case then the case distribution would also be reversed from what we are seeing as Monotreme observed approx. a month ago…

…a virus that infects mammals as if by fluke, does not spread H-H more easily than B-H…because, as Monotreme pointed out, there are more infections out from the index cases (within clusters) than overall index cases.

The point is that the only reason, in my opinion, that the virus is not going epidemic (really big clusters 100′s or 1000′s) is because it has not as yet set up the right opportunity…highly infectious person in airport etc…

…the highly infectious respiratory shedding time period is short for now. It has done most of the adapting it needs as evidenced by the clusters, all it needs now is geographical opportunity…it will grab a niche and then finish its adaption to widen its shedding, infectivity period…ie. period of transmissibilty.

Tom:

It is possible to over-think things, you know (speaking as an experienced over-thinker of things).

Being so widespread among birds, the virus is surely “picking out” huge numbers of people; it just isn’t successfully “infecting” very many of them. As Mono points out, it’s the “shotgun” method; no big mystery there.

If you find a genetically susceptible person, you get that for free. It looks like maybe someone has been spending just a litttle too much time on this; could it be time for a break? When was the last time you went for a picnic, or a canoe ride, or read a novel (by someone other than Stephen King or Robin Cook)?

If we’re talking about geographic distribution, then certainly that is better explained by the airborne delivery system H5N1 gets as a benefit of being a disease in birds. But if we’re talking about distribution within clusters, we have only so many possible explanations available. It could be exposure to a common source — which just about everyone now agrees does not appear well-supported by the evidence. It could be more efficient H2H transmissibility due to mutations in the virus — which makes one wonder why the clusters we’ve seen so far have been as limited in size as they have. The “goldilocks shedding phase” idea may have merit — but I haven’t seen any actual evidence for that presented. At this point, the bias toward blood relatives in clusters strongly suggests genetic susceptibility — but the sample set is small, and it wouldn’t take many counterexamples to undermine that hypothesis.

The race goes not to the swift, nor the battle to the strong, etc. Even if, somewhere in the world, some strain of the virus aquires the changes it needs to erupt in a pandemic, nothing guarantees that such an opportunity will present itself; it still has to encounter a susceptible human host. Even if, all across the world, humans are being exposed to the virus in ever-increasing numbers, nothing guarantees that this will lead to a pandemic; the virus still has to aquire the changes it needs in order to be easily passed between humans.

One of the very few things I think we can be absolutely sure of is that multiple factors are in play here.

Hi Racter.

If the avaliable seroprevalence data demonsrated large numbers of asymptomatic infections, I would agree with you but it does not.

Lets say I line up twenty people. The virus has no way to identify those that are genetically predisposed and those that are not. Therefore, it has to infect all twenty people, the genetically suceptible one gets the disease and dies, a percentage would get varying lesser degrees of infection and a good number would be asymptomatic…

…the serology would show indication of infections through rising titres in acute and convalescent blood samples…

…but this is not the cases. The infection is only in the one out of twenty persons in the line and therefore this could not be as a result of genetic susceptibility.

TomDVM, how many people do we assume are being exposed for one infection ? Even if it is 10 or 100, there are so few infections that the seroprevalence data can still be negativ. Or maybe the persentage of people with lesser degrees of infection is small.

Some genetic factor which prevents the virus from entering the bodycells. But why does this play no role in chickens or tigers ? When you have lots of people in a camp together with the Sumatra index-case, could that already start a pandemic as in 1918 ?

“If the avaliable seroprevalence data demonsrated large numbers of asymptomatic infections, I would agree with you but it does not. “ Tom DVM

Perhaps this is so becasue the virus is not able to infect most people at this time. Line ip 20 people and 19 have resistance. One does not and some of the person’s family members have a similar susceptibility. Some of the family also have the “usual” resistance and they do not get it or need to show any form of resistance.

Mt estimates are 1 per 32 million index cases. So suscptibility is rare for those exposed. Apparently it is continuing as clusters are not exploding.

anonymous and Joe W. Good points!!

Lets reverse the argument for a minute. Lets fulfill the requirements for genetic predisposition.

Twenty people are lined up and challenged with sufficient viral load to produce infections. Only one person develops clinical signs. We then take blood sampes 5 days and 21 days after the challenge…

…If this was due to genetic predisposition we might see seroconversion in 15–18 out of the twenty people…so that in all but one, the virus contacted the immune system producing a measurable response but the virus could go no further except in the one person with the genetic predispositon.

Secondly, the Genetic predisposition within a family should have been answered by now as the distribution of cases seem to point to it. If they have not presented it as the conclusion, then there have to be basic problems with the arguments…

…the point is that even with genetic predispositions, you do not get a distribution of 100 % infecion rates, you may get 50 % but most often it is far less…

…with H5N1 it seems to hit every family member who was in the vicinity of the index case. This, in my opinion, is not genetic predisposition but an example of a ‘super-shedder’, shedding high numbers of virus for short periods of time…

…therefore, at its intermediate evolutionary stage, this virus in some sense is mimicing SARS.

Its next evolutionary step does not require mutation first, it just requires a super-shedder to be in a hotel elevator like SARS did in Hong Kong in 2002…at that state with a cluster in the 100′s or 1000′s, it will achieve further and proabably final adaption.

A note on genetic susceptibility. It doesn’t have to be either or. Genetic susceptibility can be one of the factors that influences H5N1 infection without being the only one, as Racter points out.

Note, all infectious diseases have an element of genetic susceptibility. The genes associated with the immune system are under strong positive selection in humans and other mammals for this reason.

However, there are molecular and biological differences occuring in H5N1 which makes it more dangerous to all humans. Signs of adaptation have been observed in both the hemagluttin and polymerase genes, recently. The virus has been observed in the throats in noses of patients in the Karo cluster. This was never seen before. The virus is clearly changing. I suspect the range of susceptible humans is will get much bigger, perhaps soon.

I do not know enough about virology to create a real argument. None-the-less, rather than genetics per se. Lets say that some people are born with a specific type of receptor that allows H5N1 into the system. Most people do not have the receptor or a variation of this receptor.

From what I read and posted about the course of influenza it was found that H5N1 presents like any other virus (Indonesian physician’s comments in a news thread) and that people with influenza are infectious from day one through day 14 and beyond.

I like the super shedder argument but see no one working with these people who say say that there appears to be a time period in which a patient apears to be more infectious than other times.

Tom:

You seem to be assuming that more effective aquired immunity is what determines whether a person is infected, but infection is a prerequisite for aquired immunity; if genetic factors prevented the virus from infecting host cells in the first place, there would be no infection, no antibodies, and negative serology.

Should be presents like any other “influenza” virus.

From what I have learned lately, virologists are highly specialized biochemists and are particularly involved with cellular structure and not with the dynamics of contagious diseases and the multiplicity of factors that are involved. They do indeed take course work in genetics but they are not particularly well trained in the social conditions under which a virus spreads. This is not a condemnation of virology but a comment about the breadth of the highly technical field in which they work.

In the present discussion an epidemiologist might be better trained to comment about the spread of disease. Apparently this field of study is more knowledible about how diseases develop into epidemics. I have in the past assisted some biochemists with the development of their publications and the statistical analysis of data. In this interdisciplinary work I found that many people in the biological sciences have a working knowledge of statistics but not an in depth knowledge of the development of applied procedures. This too is not a condemnation but recognition of the idea that we all have our limits and that we often perceive the elephant from a very limited point of view. This is nothing more than the reconition that in today’s scientific worl we tend to overspecialize.

Racter I agree with you that there is an element and possibility but that is not the way they sell seroprevalence studies. The problem with that argument is that at some of the twenty people virally challenged would seroconvert…

…as I’m sure you know, nothing in science is 100% or 0% either way. There must always some, even if it is a relatively small number, in the intermediary group. We are not seeing that with H5N1 but we have seen it before…

…I think a strong argument could be made for genetic predisposition in the H7N7 outbreak in the Netherlands where all family members and many other contacts seroconverted but only one person, a veterinarian died.

There has also been discussions of genetic predisposition in certain subtypes of the human race…but I don’t think that is the case if we examine the 1918 outbreak…

…there is inherent immunity in populations, as many diseases exhibit including small pox in natives in North America. Whether that is as a result of a genetic predisposition is possible but not the only explanation.

There will always be a certain randomness with epidemics and pandemics…which will always cloud the issues and the answers to some extent.

It is for this, among other reasons, that discussions here are so interesting. There is little substitution for the experience that Tom DVM has in the field of applied medicine, the comments of virologists who contribute their technical knowledge, and the observations of others about the development of social policy. This is one hairy beast and all perspectives are needed but it would appear that no one discipline has “the” answer.

JoeW. I agree completely…who would have thought we would have the nature vs nurture debate in relation to a pandemic virus…life sure is funny sometimes.

This is a multi-factoral issue with genetics as one component. My argument is that it is not a major component to this point. The virus can’t be that good at picking only genetically predisposed without serology in non-infected family members or close contacts.

This is one funny bug…and I think also the most dangerous because, in a sense, it is predictable in it’s unpredictability.

That’s true, but at this point, the lack of intermediates could still be an artifact of the small size of the sample set.

I don’t think it’s only 1 in 20 who becomes infected. Some nurses were infected and too many family members in clusters. Even in families many should be immune with 1:20. But spread by human coughing seems to be more efficient than spread by eating or contact. So 1:20 could be for contact and 1:2 for coughing. Plus maybe the genetical factor. Whether you are a good spreader could also be genetical. Maybe good spreaders are particularily rare.


mono, the virus was in throats and noses before but in smaller doses, I think. There needn’t be a change in the virus-code. It could also be in the human genetic code which makes them having higher doses in the throat and noses.

bump to fix thread

Racter. I repectfully disagree. Serology is one thing that you will get, even in small sample sizes.

Many times, at least in epidemics in farm animals, you are working with very small test populations, partially due to out of pocket costs for serology and the fact that often the animals live or die before you get the results back.

To me it seems that the resistance to this virus must be quite strong. One index case per 32 million people (as a very rough estimate) is extremely high. When this is combined with the (repulsive) idea that some people clean the mucus from a bird’s beak with their mouth, it seems that resistance must be astonishingly high at this point. Personally, I have no problem with the idea that H5N1 is endemic in most of the world today. No one, to my knowledge, has said it but it seems quite likely that the recent Indonesian cluster may well stem from eating a sick pig that may have been under cooked. Apparently, there are many primitive and highly risky practices in many parts of the world.

While the social infrastructure is not present in many places, we should have heard about hundreds, if not thousands of people coming down with the virus given the conditions under which many of these people live. There have not been any epidemics to date and there must be some reason for this “lack” of data. In my thinking, if one considers how quickly the virus spreads among birds, the available conditions, and the number of opportunities, something strange and strong is going on.

TomDVM, can’t the virus be defeated by other things than immune-reaction ? Just some coincidences of nutrition, habits like sleeping or sports. Then you won’t see an immunization, I assume

Racter and JoeW. I guess one alternative is too consider if there is an alternative if genetic predisposition is removed from the equation (hypothetically because genetics can’t be removed from natural life systems even for dew worms).

H5N1 infects ten people but for 5 out of every ten people, those infected become super-shedders…most likely this is due to possibly undetectable virus mutations or it could be just a random appearence.

The super-shedder, sheds high numbers of virus in respiratory secretions for a short period of time, after showing clinical signs but before they would be sick enough to enter hospital…this would leave the family group most susceptible to infection…

…withing the family group some would be infected, some not due to differing viral loads, but in some cases all would be infected demonstrated high and very successful transmissibility…

…community members are not infected because the person is not infectious in the early stages and Healthcare workers are not infected because the patient isn’t infectious through respiratory means in the later stages after hospitalization. This differs H5N1 from SARS that consistently maintained its infectivity once it started.

Although the respiratory shedding occurs for only short periods, the body fluids spread continues consistently throughout the infection causing some infections.

JoeW, why 32 million ? We don’t know how many were exposed. H5N1 probably usually don’t infect in the intestine, so eating large amounts of infected meat is not necessarily large exposure. The pig-eating in Indonesia was 2 days after the coughing. Birds have other habits, they may well get it easier just by different habits.

JoeW.

‘To me it seems that the resistance to this virus must be quite strong’.

It could be resistance or it could be that the virus is not adapted to humans and that infection in the index cases may be due to measurable viral load or mode of infection or entry point.

I think Monotreme has presented evidence that indicates that the virus at this point, is quite sophisticated in its adaption…in otherwords, it is a lot further along the evolutionary path then the small numbers of clinical cases would at first indicate.

anonymous and JoeW. I don’t think the pig played a role whatsoever.

In respect to this discussion, we must always keep in the back of our minds the most important overall variability…that there is no seroprevalence data to indicate any contact with the virus other than in those that get sick from it.

Sorry, should have said ‘…the most important overall variable…’

can there be seroprevalence when you not get sick ?

anonymous. Good Point. Unfortunately in science there is little black and white.

Technically speaking, there should be seroprevalence if you contact the virus even when you are not sick…

…but I have always been with Racter on this one. If you contact the virus but the virus does not enter cells to contact the immune system, then you would not have serology.

In other words, I have never believed that contact always equals positive serology…even when vaccinated, a certain subset of the populations will not develop any immune response…this is particularly troublesome in the case of rabies vaccine.

When the Bird Flu was found in India and Africa I used the number of index cases and the populations of these areas to estimate the number of opportunities for mutation that were available.

Tom’s argument about swamping out a body with a high viral load makes sense. The super shedder in a limited time span makes sense. I guess that at this point I do not see the evidence and would like to see the epidemiologists conduct the studies to test Tom’s idea.

I think it might also be worth looking at the genetic and/ or biological structure of the individuals who have contracted the disease to determine what (if any) biological weakness the exhibited.

Given the wide geographical locations of this influenza it would appear to me that behavior has little to do with it, excepting of course highly risky behaviors as indicated in the prior post.

Hi JoeW. Did we ever do a calculation to see if we took say the last twenty cases, how many would be index cases vs how many would be secondary or tertiary.

In saying this, I don’t mean to submit you to that torture again, I just wondered.

Sorry Tom that one did not get done. And I had better take a day of rest or I will have problems with my marriage — and that could be worse than a virus in my life. Ya’ll have a fine Sunday.

Tom DVM- I had totally agreed with you that the first jump to a new species must be a random mutation, after which selection is at work for the new environment. I didn’t mean that every mammal getting H5N1 infection is a new fluke virus again. This ability became a part of H5N1 probably before the first human case. To be able to infect so many species is quite an unusual virus. As a Vet. have you heard of any other such disease that could open so many different doors?

I see Monotreme mentioned the casino effect, which is in this article, but others may not have read this. I’ll only put a few paragraphs in of a very helpful article-

http://tinyurl.com/puz6v Wendy Orient - June 4

Right now, the H5N1 virus is beautifully adapted to chickens. Researchers want to know more about the process by which it might become adapted to humans.

Part of the problem is that “mutate to transmissibility” means different things to different people. To Peter Palese, chairman of the department of microbiology at Mount Sinai School of Medicine, who has studied influenza viruses for 35 years, the phrase makes sense. “These mutations [to make the disease transmissible from human to human] could happen in a chicken. It’s not likely, but it cannot be excluded.”

To Brown, H5N1 mutations are not enough. They have to occur in the right context. “It’s hard to get infected with this virus,” he said. “You need a large dose of it to ensure the presence of some mutant strains suitable for growing in mammals.” According to Brown, several different mutations on different genes seem to be involved in a virus moving from one host to another. Bird flu strains he’s passed through laboratory mice have changed in ways similar to what has been seen in certain cases of the human H5N1 virus, suggesting that the changes may be significant for the strain’s adaptation to mammals.

Some mutant strains have appeared repeatedly and independently in different humans infected with the bird flu virus. In one patient in Turkey, about half the H5N1 strains detected appeared to be viruses that had adapted to humans. But, as Brown points out, the changes were a dead end — the victim died without passing on the disease.

The bird flu virus is still at the starting gate when it comes to humans. But should any strain of H5N1 manage to survive many sequential transmissions, Darwin’s charioteer may drive off. The best transmitters will be favored by selection, as evolutionary biologist Paul W. Ewald of the University of Louisville contends. The process will continue, human by human, until a fully human-adapted, explosive strain emerges.

This process of adaptation is probably how pandemics begin.”

NJ. preppie Thanks for the information, I had not read any references concerning the casino effect.

Actually, I think we could concieve multiple doors each corresponding to different species each with a hole in it and H5N1 entering and exiting randomly.

I kind of concieve it as disorder (chaos) changing to order…the order phase due to Monotreme’s et al’s selective adaption…we are probably entering that phase now.

As far as your question goes, I could and would never have concieved of a virus of this unique ability. Many would not understand just how unusual it is to infect so many different species of animals…in effect several separate jumps to separate species at the same time…

…This coupled with an astounding virulence, I believe not seen since small pox or the plague…and probably the potential to be more virulent than both. This is potentially a one in a thousand year predicament.

All I can say is they had better be right about that species barrier…except I think that argument ended in 1997…It jumped the species barrier then, didn’t it…and has done so repeatedly in several distinct locations with increasing efficiency…and worse in several species…UNBELIEVABLE. I don’t know how they could hold onto that argument at this point even though I wish they were right.

Veterinary Medicine is full of virulent viruses that would not be understood by human practioners. A very good example is canine distemper virus that has also crossed to other species. We discussed zoonotic diseases during vet school but they were not an overwhelming concern…

…I live in the highest rabies incidence area in the world so that was a major concern…Leptospirosis, a bacteria, was a concern as well as standard food poisoning such as salmonella…

…influenza wasn’t even mentioned and I think that says it all.

There is very good reasons here to be very worried about the near future, in my opinion, but once again, I hope I am wrong.

Thanks for asking the question.

Thank you for the zoonotic viewpoint. It’s hard to believe that people, scientists even, can look at this virus and what it’s doing, and say it’s very unlikely to become human adapted. Yes, we know it doesn’t happen anymore often than a few times a century, but if ever there was a candidate, what do you expect it to look like? I think it looks like a duck and quacks like a duck.

My point about selective pressure is that people often use the concept to say there’s no reason for the mutation, that’s why it’s unlikely. First there was no need for the low path H5N1 to go up to a high path virus. The battery cage farms allowed the change to happen, but dense passage doesn’t always cause the same result. Many other Avian Influenzas have gotten into dense chicken farms with different outcomes. Monotreme said it was created from bad vaccines. Would bad vaccines do that every time or was this an unique result? It may show the path the virus took but doesn’t mean it was pressured into these changes. H5N1 was a super-successful bird flu, why did it need to infect the first cat, the first human, and many others. It’s possible but not normal or neccessary. Yet in the face of these cross specie transmissions, some experts will say there’s no reason, unlikely, that it’s going to adapt to humans. Why I harp on this is because these opinions intimidate others in communicating the danger thru the media. It’s a scientific fashion to be neutral sounding; intellect overules emotion; only nuts sound fearful. We have to hope the development of H2H goes slow enough that there will be time for more people to understand what is coming, through repeating containment efforts generating big news.

NJ Preppie. I pretty much agree with everything you said.

At the end of every discussion we come back to the crux of the matter…as Monotreme first observed, why does this damn virus spread better H-H than B-H…more in the clusters than in the index cases.

From an adaption point of view, this is a tough one to sort out. It’s poorly adapted for the first jump but very well adapted for the second.

We have got a little off the original topic of the thread so one hypothesis could be, like SARS, that there is an intermediary mammal and the birds and just a ‘red herring’…hey, I think thats a joke!!

I did not want to infer in previous posts that genetic variables are not involved. In fact, the apparent propensity to children could be due to higher metabolism leading to higher internal lung temperatures. Co-infections of children with other viruses would also increase body temperature mimicing the genetic effects…the virus is accustomed to higher body temperatures…

…there are a multitude of possibilities from the genetic perspective, it’s just that specifically the clusters aren’t explained by genetic predisposition in my opinion.

In a sense it doesn’t matter if H5N1 initially infects humans due to unique genetics or due to co-infection with another disease like HIV or due to unique exposure. The key point for me is the passage of the virus from one human to another. When virologists want to adapt a virus to another species they passage the virus from one individual to another of the target species. This almost always results in strain of the virus that is becomes adapted to the target species. Sometimes evolution is very predictable. One or two passages in humans of the pure bird H5N1 is probably not enough “time” in humans to produce a human adapted virus. However, an intermediary mammalian host may reduce the number of passages in humans that is necessary to produce full blown human adaptation. This is why H2H2H in Karo cluster was so alarming to me, and I suspect, to many virologists. Some of which may have contacted TPTB.

Would the blood tests of the people who have survived have all of the sequences that Dr Niman needs? Just wondering if we could PAY one of them to give a sample that Dr Niman could analyze? Or is that a silly idea?

for the experts this shouldn’t be so new. WHO,CDC,.. are pointing this out now : we had it earlier. We are still waiting for a report from the Dutch group to examine Indonesian cats…they are not withholding this, are they ?

gharris, the blood only has antibodies, not the whole virus. You can’t conclude a lot from the antibodies. Better ask the people when they are sick for an additional sample to be sent to an independent lab. ! Hmm, would this be illegal in Indonesia ? Can’t we just offer money for the samples, so people can send them to another lab. too and get paid ?

why doesn’t the Indonesian strain travel ? It’s still only in Indonesia. Maybe it can’t well survive in birds elsewhere ? Maybe it couldn’t well go pandemic in humans because it needs the Indonesian climate or some special animals to spread it ? The Qinghai strain was much more successfull to travel.

Speaking as a complete non-scientific person who has followed this for several months, here is another question: Why have the influenza’s been labeled “avian influenza” at all? The more you look at the influenza’s, the more you realize they are not particularly avian - and in fact avians may not be the main host at all. You have H3N8 which was supposedly equine, now also canine. You have H5N1 which appears to affect multiple species. The concept of species barrier does not seem to apply to influenza at all. Maybe we have been misdirected by presuming these were avian diseases in the first place. These influenza’s may have been present in multiple species for thousands of years, and we just were not looking for it.

with 200 miilion birds dying from H5N1 and 200 humans 150 tigers, some cats etc. it is clear that the priority is on birds

I think that is only because the habit of birds is to flock together - and of course we have artificially kept birds in large numbers together in agribusiness. I don’t know the breakdown of the 200 million, but if we took only the wild birds that have died I think it might be a lesser number. The tigers were also being kept in close proximity artificially in a zoo. I would suppose the same would happen with any species kept in large numbers with close quarters - humans included.

no, other animals also flock together. And a great variety of birds are infected. Yes, most of the 200 million were chickens, but we still have a large factor with wild birds vs. other species.
species

petperson – at 02:55

You are asking the right questions. The concept of a species barrier is just that, a concept.

As we are dealing with a promiscuous organism in a very forgiving and fluid gene pool, expectations of genetic acquisition are almost always met.

We can isolate certain strains that will only grow well in certain species, but that, in itself, does not constitute a species barrier.

Avian, murine, porcine, canine, feline, human influenza, call it what you will; in the end, its a new killer on the horizon and has little concern for its victim’s species classification.

For that matter, the concept of species is itself just a concept.

petperson. You raise some interesting points. What would have happened if we had taken the last index case, the woman in Indonesia, and placed her in the middle of 50,000 people jammed into a stadium meant to hold say 30,000 (Katerina). Would we have observed a different subset and patterns of infections.

I agree with you. Birds are particularly sensitive to respiratory viruses because they have evolved massive capacity for air exchanges but the primary infection pressure is the population gradients that they find themselves in. If the humans were in a similar state then it would probably be called homo sapien influenza.

I went back and read Monotreme’s initial post because I think we may have gone off track, not necessarily a bad thing.

There are a couple of issues. First, the question is whether viral evolution progresses in a steady progressive fashion or does it have the ability to leap…adaption all at once to another species.

Then there is the question of whether another mammalian species is assisting in the adaption of H5N1 to humans. If this is the case then the pig would seem the most likely candidate. Pigs live in close association to poultry on farms. In addition, pigs are kind of the garberator on these farms, whether the farmer wants them to or not. Pigs are also quite inquisitive and smart animals. So if poultry are infectious, pigs will be in close enough contact to be infected. If poultry die, pigs would more than likely eat the carcasses and there could be contact through manure as well…

…The most dangerous mammalian intermediary vectors would be ones that are completely asymptomatic, as in the Civet cat and SARS. We have not seen outbreaks on influenza in pigs. Influenza in pigs did not exist until 1918, when humans infected pigs…it has been in pigs as swine influenza ever since…

What if pigs are naturally resistant to influenza, not being infected before 1918, and therefore are asymptomatic, able to constantly passage the virus? How would this affect the adaption of H5N1 to humans?

And last, we still have not come up with the answer for why the intial case from avian to humnan appears more difficult now then the spread between humans. I think it essential that we come up with an understandable explanation of this…because in the anwer is how much time we may have to prepare for a pandemic.

Sorry, I guess one final question would be…What if we took the woman in Indonesia, the last index case, and put her in a Hong Kong Hotel, thinking she was suffering from a cold?

Tom DVM - 12:55 Somethime you need to go backwards to move ahead. Just currious, but why haven’t scientist gone back to the lake where they think the BF started and tested everything around it. It seems to me that something their is continueing to infect the birds, but what is it? That is if this is ground zero. gina

the lake is just one place. The Indonesian strain didn’t come from there. H5N1 infects birds in the intestine, not respiratory, I think.

Mono (in this thread’s OP):

I agree. The concept: “Natural Selection” is in general somewhat subject to abuse, and biologists themselves are often among the worst offenders.

Well, that conclusion is clearly flawed, by whatever path it is reached. More forgivable, though less transparently flawed, would be many conclusions based on the assumption that one may confidently trace the path by which a particular location in evolutionary design-space was reached — i.e, that if some organisms survive while others do not, selective pressures must be the reason, and the exact nature of those selective pressures should be intuitively obvious given the proper frame of reference. The idea that selective pressures (while it thrives in other host species) could drive the virus toward better adaptation to humans is at least theoretically defensible. All that is required is to invoke what Gould called “exaptation”; the idea that structures driven by selection toward certain forms could serendipitously find new functions (bird feathers originally served as insulation, etc). Supporting the mammalian reservoir hypothesis empirically would involve establishing that “adapted to humans” and “adapted to [insert species of choice here]” are close neighbors in local design-space (which certainly involves receptor binding, and possibly who-knows-what else).

Anonymus - 13:51

How can we be for certain without the all the sequences? TPTB are overlooking something. I believe that is why they are at a croosroads. To many loose ends? Step back and look at the big picture. gina

Racter - thank you for the rewording wording of the point. Evolutionary design in regards to animals is different due to the time refinement process. Animals are honed to fit a niche. That leads to understandable extrapolation towards a virus evolution. But the rapid mutation of a virus needs a separate consideration. The accidental designs are fleeting but possibly deadly, and purpose of lethality and neccesity, not that relevant to its procreation, which may be fleeting. We see the possibility of both, jumps over to mammals, developing in reserviors, gaining successes, and basically knocking on the doors until it gets in.

Backtracking in this investigation, here is another question. How do we know - or do we know at all - that the sequence going into an animal is the same as what we later analyze coming out of the animal? Maybe the sequence is developed within the particular animal. For example, trying to make this hypothetical question comprehensible, let’s say there is only one core influenza virus - let’s call it X.

Could it be that when a bird contracts X the virus develops inside the bird to a sequence XZ; or that if a pig contracts virus X the virus develops inside the pig to read as a sequence XY, or inside a human as virus XA. And maybe only after that conversion within the animal can the virus transmit to other members of that same species, dependent on close proximity of high numbers of the species.

Do we know if what virus goes in is the same as the virus that comes out? Maybe the sequences are not the beginning of the story.

Petperson- Right, the adaptation do show up in a lab mice and in people sequences. There are different winners from the initial bird virus strain. In the link below, notice the idea that the initial “load” of virus needs to be high, in order to recieve enough mutants, for human infection. This is one more factor to clusters. Once a match is made between susceptible host and viral load, then the index case is producing more of the human oriented mutants. Then the H2H transmission becomes easier than the first acquired infection.

http://tinyurl.com/puz6v

“To Brown, H5N1 mutations are not enough. They have to occur in the right context. “It’s hard to get infected with this virus,” he said. “You need a large dose of it to ensure the presence of some mutant strains suitable for growing in mammals.” According to Brown, several different mutations on different genes seem to be involved in a virus moving from one host to another. Bird flu strains he’s passed through laboratory mice have changed in ways similar to what has been seen in certain cases of the human H5N1 virus, suggesting that the changes may be significant for the strain’s adaptation to mammals.”

I’m a HCW not a vet but I found the concept of the super shedder fascinating and it fits the currrently known data. But my question is this: The species barrier—could it be eroding or undergoing change? The reason I ask this it that it’s thrown out often when you have a sick pet, but how to you know for certain it’s the same as it was fifty years ago? Human DNA is changed by a virus, it must be the same for other mammals. Who’s in charge of monitoring shifts in the species barrier or is it just considered a done deal? My personal thought is that it is changing and perhaps the barrier shield we think is there is only a figment of our imagination.

Leo7. The term super-shredder may be slightly misleading. I couldn’t come up with a more appropriate term.

I think generally H5N1 in humans has been limited to body fluid transmission.

However in the index cases in these clusters, I believe they are shedding virus in the respiratory tract in the same way as a cold or seasonal influenza. I didn’t mean that they were shedding abnormally high amounts of virus although they could be.

What appears interesting, is that although the index case is infectious through respiratory droplets, the later cases seem no as efficient and respiratory transmission does not seem to occur in the later cases out from the index case…go figure…just another connundrum presented by this weird virus.

Tom DVM at 18:21: Might not that “conundrum” be the key to telling us how soon we could be expecting Stage 6 from this “wierd virus”? If Niman just had the sequences!!!

Medical Maven. I agree. If we could answer two questions, we could foretell the future with some accuracy.

First, why is H-H more efficient then B-H, in other words why are there now more secondary cases then index cases.

Secondly, as you said our ‘connundrum’. Why would an index case spread by respiratory droplets while the rest of the secondary cases not spread by respiratory droplets…if the virus had mutated, you would think the mutation would be in the secondary cases.

In these two problems is the key to transmissibility.

…and then there is the third and probably most important problem. It appears that modern science does not have a clue about what changes occur in a virus to increase transmissibility. It seems we concentrate on the N and H segments while there are six other genes that must play some role…

…so as you said M.M., even if we get the sequences, I don’t think we know enough to tell for sure one way or another. We could concievably be told, as in Indonesia, that no significant mutations have occured when they don’t know what a significant mutation might be in regards to transmissibility.

It seems we might be in the dark until the virus turns on the light for us and two in the morning just after we have fallen asleep.

Tom DVM at 19:06: One of your best. And I am ashamed to say that I laughed out loud at your last statement. I guess if you stick with this site you have to have an affinity for gallows humor. I would put that last analogy of yours in the “top ten”, (we need to do nominations on these off-the-cuff gems). : )

Medical Maven. Thanks.

From MaMa – at 21:22 on the News Thread

People’s Daily online- “The Chinese government should review the strategies and effects of the bird flu control efforts of the past two years and improve them to cope with the epidemic which is still a serious threat, said a Chinese scientist in Beijing on Monday. “When, and to what extent, the current avian influenza virus could evolve into a human pandemic is unpredictable. We should do our best to reduce the risk of a human pandemic influenza breaking out and make necessary preparations before such a risk becomes reality,” said Chinese bird flu control expert Liu Xiufan…”

…”Some changes in the H5N1 virus have taken place recently. The virus has increased virulence to ducks, and the currently available vaccines are not effective for protecting poultry, said Liu.

The H5N1 viruses isolated during the 2004–2006 period have increased their ability to replicate in mammalian cell culture. The transmission mode of the viruses is changing from fecal-oral to aerosol, said the scientist, adding that the viruses have increased resistance to the environment, especially to temperature.

He noted that it is a big challenge for China to eradicate the H5N1 viruses because the viruses have been circulating in poultry in China for some time. The outbreaks of bird flu have affected vast areas of China. The extensive presence of waterfowls and vaccinated birds as the carriers of the H5N1 virus has increased the difficulty of effective control and eradication, Liu said…”

more…http://tinyurl.com/hbtto

I think this is relevenat to our discussion here.

Monotreme. Thanks…and we thought it would be Indonesia…never underestimate the melting pot!!

Leo7. Your question on the species barrier is an excellent one. I don’t know how to answer it other than to say…what species barrier? It seems like we should throw out the rule book because both viruses and bacteria are jumping it in a multitude of species all over the world. Seems to have been going on for approx. a decade.

This is from a article Kent Nickell found. It is on Kent’s thread Host Range and Pathogenicity.

Host Range Restriction and Pathogenicity in the Context of Influenza Pandemic Gabriele Neumann* and Yoshihiro Kawaoka*†‡

University of Wisconsin-Madison, Madison, USA; †University of Tokyo, Tokyo, Japan; and ‡Japan Science and Technology Agency, Saitama, Japan

“Although all 8 RNA segments of the Spanish influenza virus have been sequenced, these sequences offer no explanation for the high virulence.”

Tom DVM at 18:21-I can hold super shedder in my thoughts quite easily and I found it appropriate. Your disclaimers noted. See article posted by Monotreme re:China. Interesting they held the key in silence isn’t it? I remember just before the Google problem began with China—some reports leaked that BF was in villages in humans but it was never vindicated. That country is locked down and no reports will be leaking. In made me wonder though… 5 to 1 has gotten a lot of practice time in China preparing for the audition.

Just an observation — fecal/oral is a fairly efficient way for a virus to spread. Hepatitis, polio, typhus …

I’d love to hear a clarification on the fecal/oral route they hinted at. Is it going h2h2h2h2h2h2h2 … fecal/oral? Or just bird-to-human via fecal/oral.

Given the fact that people could hypothetically shed virus in their feces a long time after they recovered from any obvious symptoms, this could explain why small clusters keep popping up in absense of an animal exposure. i.e., someone had H5N1, recovered, and now they’re a typhoid mary. It could also explain family clusters quite neatly.

Maybe one of the experts here would like to speculate on that? Am I off base?

Disgusting to think about, but fecal/oral infection happens fairly frequently even in our modern world …

Leva

when they say fecal-oral , it doesn’t necessarily mean, that the virus infects in the digestive tract in the first place, does it ?
Cygnet, the article says H5N1 is moving away from fecal-oral towards aerosol.
These virus changes 2004–2006, can it be demonstrated by the sequences and mutations ? I’d like to see that.

anonymous – at 05:46 These virus changes 2004–2006, can it be demonstrated by the sequences and mutations ? I’d like to see that.

Me too.

Moving toward multiple routes, not necessarily moving away from fecal.

• Fecal / oral
• Respiratory

My hunch at this point is that it may be both now, fecal/oral and respiratory, in Indonesia and perhaps China as well. The R0 for the respiratory spread is still probably below one. This may change very quickly. I will echo comments on other threads: Now is not the time for complacency. We are being given multiple signals that the virus is evolving towards a pandemic strain and that there are clusters that are not being reported.

is there any fecal-oral with normal flu or 1918 H1N1 ?

Start weighing the fact that many of us are having that same hunch and you get a full camel-load of hunches.

May not make any of us right, but it sure makes us watch carefully.

anonymous, all flus start out as fecal-oral, in birds. No-one knows for sure how avian flu viruses adapt to humans. The last time this happened was 1968.

NS1, we are working with incomplete information. However, the human brain evolved to make predictions based on incomplete information because if we waited for complete information on key survival questions, we’d perish before we reproduced. I agree with your statement about a growing consensus. Even former flu skeptics like Wendy Orent now accept that evolution may favor a pandemic strain of H5N1. I wish someone would make this clear to TPTB. Even though they’ve been briefed, I still don’t think they get it.

Monotreme-

I don’t think that they will be able to get it until they have gotten it.

Until a large portion of a nation’s people have H5N1 coursing through their veins, most politicians will likely be in denial, a very well-justified denial for their self interests.

Consider the political cost of compliance to the idea of a pandemic with immediacy. Immediate action would be required. I don’t think that these folks can afford to take decisive, immediate action because the risk of being off in timing is high.

Sad situation if PF51 hits soon because so few will be notified and prepared.

I don’t think they will be able to get it until they are presented expert probability estimates as in 1976.


Is it more effective for flus in humans to go for both, fecal oral and respiratory or won’t the more successful viruses specialize in respiratory ? So, for H5N1 adapting to humans won’t we expect a specialization in respiratory transmission ? It seems that these are the only ones to cause pandemics. (except some slow pandemics like AIDS

Respiratory effluence is typically a more efficient vector than fecal effluent. The fecal route will likely continue as a vector, just a less important vector.

Failure to reset my Author title effluence is a more efficient vector to indicate that its time to go to bed.

I don’t think it’s actually fecal oral in h2h. Maybe droplets→food→oral. Or directly by coughing. Did they all cough in the clusters ? I think coughing is (was) not typical with H5N1. (?)

Thought this letter from a woman in Indonesia might give you some insight as to the situation there. Seems that “six degrees of separation” is a truism. When I emailed my sister about the recent H2H2H situation in Indo, she emailed it to a friend who then emailed it to THIS woman in Indonesia. And this is her response:

“Thanks for dropping me an email. feel touch by your concern for us in Indonesia.

Yes I did read about this case on news paper. In fact there is alot of case related on bird flu pandemic. Since last year, we had been frightening by this pandemic as there is more people died of this disease. When it first started, people are avoiding to eat chicken, duck, pig or bird. But then after sometimes, people is become less care Maybe because we are tired of getiing worry.

Our government is very slow on taking any action to prevent this pandemic to be spreading

They are too busy with so many problem we have in Indonesia. Pity the people who live in Indonesia. We don’t get our right to live peaceful and convenience. I sometimes envy with the european or American people where the government is very concern on their welfare. For example, when the tsunami hit Thailand, the government of europen country are busy sending flight for their citizen to get them out from there.

Indonesia is just developing country with so many people to taking care :((“

The human perspective on living in the midst of mutation-land.

Racter at 13:57 “..that if some organisms survive while others do not, selective pressures must be the reason, and the exact nature of those selective pressures should be intuitively obvious..” That is what we are not too good at doing, in regards to species barrier crossing. We can see in hindsight better than foresight. Go back ten years and who could have predicted all the rare changes H5N1 has made. Scientists understand how selection has worked in regular influenza epidemics. They also study viral mutations in laboratories. The pool of researchers with live cultures of H5N1 is limited. Experiments are complicated by the fact that mutations accumulate that are adapted to culture and lab work. The best source of the evolution of a virus into a new type is out in the field. We are missing the opportunity by not taking a lot more sequences from many animals, from different locations. We have gotten a few snapshots from a few pigs, dead chickens and humans. We are asking the question here, about mammal reservoirs, because the answer in not out there, in the published papers, as to how this mammal adaption has occured. We can hope that the research will be published explaining the next pandemic process, but it’s looking very quiet so far. Do the few sequence holders, such as Lui, Pieris, have enough information from their labs to discover all the answers?

My apologies for only being an ignorant reader, but this paper is recent -Feb 2006, from the Proceedings of the Royal Society. Title- “Epidemic Dynamics and Antigenic Evolution in a Single Season of Influenza A”

http://tinyurl.com/l3z6e

On page three, a graph shows the rate of antigen change. During a 116 day epidemic of a new variant, 5 amino acid mutations occur, when the normal speed of antigen drift should be two amino acid mutations. The greatest amount of change happens before the peak of the epidemic. With a new version of the influenza there is an intial burst of freedom in immune escape. At the other end of the spectrum, there is another type of increased mutation rate, coming from strong host immunity. So after a long slowing epidemic, when many people have immunity to the old strain or are vaccinated, the challenge increases the mutation rate, which brings about the needed new flu strain.

The response to greater challenge makes vaccinations a possible cause of greater antigenic drift. Monotreme mentioned the belief that bad vaccinations, in chickens, developed the high pathogenic form of H5N1. That shows how little they understood in predicting viral evolution, and how we got into this mess. This paragraph is from page 8 of the link above—

“Public health officials may wish to investigate whether the benefits of vaccinations during one season conflict with the feasibility of vaccination for the following season. If antigenic drift is indeed greater in more immune populations, preparedness for influenza pandemics, may need to include vaccination strategies for the second year after a pandemic with consideration to the effect this will have on the third year after a pandemic.”

NF. Preppie. Thanks for the paper. We can add it to our library of relevant articles.

I really hope that we can, at some point, come up with reasonable hypotheses for the two issues I raised in my post at 19:06.

Sorry NJ, I guess I need stronger glasses.

NJ

These mediators, like vaccination and anti-virals, are understood to drive a higher rate of change in the viral strains.

Thank you for bringing this article into the discussion.

Few really see the implications even when presented with the graphs.

Hi everyone. I went for a run this afternoon and was thinking about the two issues left to answer.

I believe there is only one possible answer to the question of why the virus is now spreading H-H more efficiently than B-H.

The only explantation that makes sense is that the virus is better adapted to humans then it is in the species it is infecting the index case from.

H5N1 has an incubation rate of 2–5 days. WHO has been continually expanding the incubation rate un to an astounding 17 days at last count…but all they are doing is knocking another hole in their credibility and insulting scientific principles and the intelligence of those who pay their wages.

We have agreed that several members of the same family would be in the general area of the sick secondary host. Therefore, if the virus was well adapted to that species, you would expect it to shed high numbers of virus and the several humans would be infected…

…but we do not see several cases that could be called the index cases: infected in 2–5 days. I believe this is because the virus is not well adapted to the animal and therefore it does not shed a high enough load to make several humans sick at the same time.

However, when it eventually gets in a human, we see now more and more clusters…and many more secondary cases away from the index case…demonstrating an improved transmissibility over the first jump from animal to human.

Monotreme, I said that thread you produced a month ago was like a ‘two by four to the side of my head’.

The implications are staggering unless we are blindly going to follow the hypothesis that since it hasn’t happened, it’s not going to.

Tom, only additional item with more of an engineering background to add to that theory. I would see, as a layman, would be the lung capacity of the animal host and total lung surface area from which to shed viri as critical. With a pig, it would seem more likely to spread airborne, but with a bird you would have limited respiration volume, so it would seem that the virus just would not be expelled in as great of a volume.

Hence, the human lungs pumping about 2 liters a respiration cycle would pump a lot more viri into the air. That to me ultimately leads to the same conclusion, however, because the virus adapted to infect a human is more plentiful around other humans. I think that is the secondary reason for the increased transmission to clusters now. It’s all about volume.

Now that I wrote that, it scares the crap out of me!

This is how the jump occurs! More viri per infecttion with more chances to find a secondary hoste and mutate, all because of volume.

Ventilation may be the key to slow this beast down!

TRay. You could very well be right. It is the difference in training between you and I. I am trained to look at phenotypic expression and you are probably trained to look at mechanics, for want of a better word.

By the way you are right about pigs…very quiet breathers…but they do have big lung capacity.

The thing is that we have been told that the virus is more adapted to the infecting species then us but that can no longer be the case, as of a month ago when Monotreme noticed what he noticed…

…if it was we would see more clusters of index cases rather than clusters outside the initial incubation period.

It would seem to me, on a purely chemical level, that the virus infecting a human would be more suited to a human. So if more of these viri are in the air, the likelihood of finding a suitable human host, especially if they are genetic family members, would be chemically more vaunerable to the virus as well. One more, just a mechanical angle. But I think this exchange of viewpoints is opening my mind to things.

So much for a complete thought, teach me to talk on the phone and post at the same time. I meant to say that “So if more of these viri are in the air, with the likelihood of finding a suitable human host - especially if they are genetic family members, would be chemically greater as the secondary hosts would be more vaunerable to the virus as well.”

I’ll keep working at complete thoughts while in isolation.

The analysis and discussion here, on the paper cited re the disadvantage of vaccination, seems to indicate that the virus changes behaviour due to a change in the host, specifically it mutates more rapidly when the host is vaccinated. I respectfully suggest that this is reversing cause and effect; That the change in result is simply due to the differing environment.

That is, the virus does what it always does, imperfectly replicate itself, but because the HOSTS are more resistant, the only virii that survive to further replicate are those that have made the needed and more extensive changes required. It makes logical sense that this difference should be so, as it is less likely overall for a virus to make 5 changes than 2.

Tom DVM – at 18:21 “The term super-shredder may be slightly misleading. I couldn’t come up with a more appropriate term.”

I suggest “mutant filter / factory” instead. This might better capture the notion that essentially the Index person receives the totality of the animal host’s viral mutant swarm, filters out all those that can’t infect humans, and then replicates the human capable mutants that can be passed to others in a large-quantity purified form.

Ignoring the issue of what to call it, though, I believe your theory is the best explanation yet as to why it appears to be more easily passed H2H than B2H.

I think we are all putting together part of the same Lego model here.

A virus survives if it can replicate beyond one generation; the more replicable virus in an area, the more likely it can find a usable host; the closer the genetic compatibility between hosts, the easier to replicate in a secondary host with less filtering.

So a “super shedder” would have to be a genetic family member in early clusters as the virus “tunes’ itself, then the later generations can work on adaptations within the specific species.

In nuclear reactor theory we talked of having the proper attenuation of a fast neutron, which is a neutron with too much energy could not bind to another atom, so no fission occurred. Once you get the neutrons slowed down, they grabbed hold of atoms and fission began.

So if the virus is “tuning” itself with each cluster it would be likely only a matter of generations before a natural mutation/reassortment becomes more attuned to any human DNA, not just a specific family cluster. The next generation of “super shedder” would be a danger to unrelated people around them.

So that would explain the flares of clusters that die out - but the moment the attenuation is right, if the host is asymptomatic for a period of a day or two, we have the flame begin. This thing is getting closer each time a cluster flares, we just don’t know which one and where the last tweak will come from, but if we already have 3 hops (H2H2H), it can’t be too far from the final phases.

Tom DVM …that thread you produced a month ago was like a ‘two by four to the side of my head’.’

Mine too. Still wrestling with the consequences. Nice discussion of hypotheses on this thread. So many possible variables that affect transmission.

One other issue I’d like to emphasize is progressive adaptation. I would predict that the virus in the last person infected, at the end of the H2H2H, is the most dangerous as it has had the most opportunity to adapt to humans. Fortunately, it has not had enough time, yet.

I think the issue of ventilation is an important one. Most of the secondary infections probably occurred when many family members spent a night in close quarters with the index case. What would have happened if the tertiary case had been cooped up with alot of people when he was shedding virus? Don’t like to think about this.

I like the idea of the mutant filter/factory. That’s a useful way to understand progressive adaptation.

Tom DVM …that thread you produced a month ago was like a ‘two by four to the side of my head’.’

Mine too. Still wrestling with the consequences. Nice discussion of hypotheses on this thread. So many possible variables that affect transmission.

One other issue I’d like to emphasize is progressive adaptation. I would predict that the virus in the last person infected, at the end of the H2H2H, is the most dangerous as it has had the most opportunity to adapt to humans. Fortunately, it has not had enough time, yet.

I think the issue of ventilation is an important one. Most of the secondary infections probably occurred when many family members spent a night in close quarters with the index case. What would have happened if the tertiary case had been cooped up with alot of people when he was shedding virus? Don’t like to think about this.

I like the idea of the mutant filter/factory. That’s a useful way to understand progressive adaptation.

Graet discussion and ideas. I think you guys are on to something. Assuming the foregoing is true it would appear that quarentine is the answer to making some strain burn out. In addition the need for full gear respirators is also implied.

One thing I’d like to point out about super-shedder’s, some are made not born. What I mean by that is that in SARS most of the time super-shedding events occured under peculiar physical circmustances. Many occured in hospitals during intubations or the use of nebulizers which aerosolized droplets and spread the virus very efficiently to many people. When this was realized and proper procedures and PPE used, the number of SARS cases dropped dramatically. Other super-shedding events occured in large apartment buildings or hotels where, again, material containing the virus was aerosolized. It happened in a Hotel in Hong Kong, presumably when the dried vomit of one of the victims was vaccumed. It happened in an apartment building where one of the victims had diarrhea. Improper plumbing and venetiliation is thought to have spread the virus to many people.

Something to think about.

I did not see this in photos from 1918 and have not seen it in pictures of hospitalized patients now, but this hypothesis also implies that infected, or potentially infected, people should be wearing masks of some sort. Sure some virus will escape but the transmissibility will be cut down substantially. I wonder why this has not been thought of before now?

JoeW, I think any hospital worker involved in intubation of a H5N1 patient should be wearing a Powered Air Purifying Respirator (PAPR). We’ve been lucky so far, but I wouldn’t count on this luck holding. There’s a reason why everyone is watching what happens to health care workers.

JoeW, it is supposed to be SOP for every patient suspect of flu, everyday ordinary flu, to wear a surgical mask to prevent transmission. The fact that this is not happening with H5N1 patients is very disturbing.

Nsthesia at 11:09 -sorry to miss your post while I was writing and ran off. Very insightful letter for a citizen to write about the difference in their country.

LMwatbullrun- The paper was the real measurement of real seasonal human influenza and that was the main discovery of the paper; the flu virus does change it’s mutation speed of antigens. The fact that it changes fastest “after” it becomes a new epidemic, before it peaks, is a little harder to understand, because it is dealing with lesser immunity in a host. It sounds like when a new variant first travels the small number of hosts lead to greater successful mutations, which is the opposite of the pressure selection that happens when the population gains immunity, then the rapid mutation rate succeeds again.

This would pertain to the antigen drift of cross species transmission, where the virus is capapble of picking up new changes faster under new circumstances. If there is another cluster under poor surveillance, where it does not get stamped out, it can make more rapid mutations than normal. That’s a little different than the thinking that it’s well adapted to birds so it won’t “need” to do that, as if it has to be forced to survive over a long time period.

TRay75 and Tom DVM - Is the mutant swarm coming from pigs breath for human infection? Not that I mean for every time a person gets infected,it just came out of a pig, but that originally it could have adapted to mammals (&us) in pigs. H5N1 could go in the pig, (from bird guano) as a bird receptor a 2,3 type. Some of the mutants start getting into the pig’s a 2,6 cells. Both are brewing along, but the upper respiratory cells favor blowing out the mutants that come out of the human type a2,6 cells. Evidently, this mammal adaptian is successful in transmission to chickens too. From the pig reservoir, many birds and mammals can get infected by this crossdresser virus. Maybe there is a high rate of producing mutants of either persuasion with each cell generation, a flexible trait from living high on the hog.

Now this is dumb, really dumb, and you need to think about it for a minute after you get done laughing.

I am not impressed with N95 masks. Transmission through the eye if nothing else. They may be cheap but they do not work well and there aren’t enough anyway.

I have a respirator with dual filters that I use when plastering and it fits tightly. At the end of a day after sanding plaster, I will have some plaster dust in the mask. Therefore, I am not all that impressed with respirators for the flu. Let alone the cost (about $30.00).

It seems to me that there should be some inexpensive method for protecting oneself and here is what I have designed. A real “tinfoil hat” idea.
A baseball cap with holes in the bill and a battery powered fan is placed on the head. Something like a colander is placed (sewn into) the top of the ball cap. A clear plastic bag with a hole in the top is placed over this contraption and tucked into the person’s shirt. The hole in the top could have cotton or some similar material as a filter. We are talking serious tinfoil hat here!

Here are the advantages.

1. If the virus is aerosolized in water drops, the drops I assume (someone correct please), have a tendency to fall to the ground.
2. The hole is in the top so there is less likelihood the virus will enter the mask from above.
3. There is no way the virus can enter through the eyes.
4. Anyone can make a variation of this design for next to nothing.
5. All that needs to be replaced are the cotton and perhaps the bag.
6. It will probably ward off little green men as well.

Would it work ???

What about laboratory PPE suits with head gear, might look a little more professional. LOL - you are talking about going out in public with a colander, plastic bag and fan on your head? Post a photo when you have it made.

Placed one on Kay (my wife) and laughed for five minutes. But what if PPE suits are not available for the average Joe? OR what if they don’t have enough to go around in the hospital.

Kay says that any credibility I may have acquirted on FluWiki is now gone. Oh well, didn’t have any to begin with.

JoeW- http://tinyurl.com/lcfdy - spring for one of these, you’ll look so snappy.

JoeW-

This is the kind of creative thinking that we need. Field expedient and safe when nothing else is available.

Please tell us what Kay says when PF51 hits and she has all the latest and greatest self-developed tools.

JoeW - I know what you are saying however about your tin-foil hat. In a situation, you have to use the available resources you have.

I, too, see the N95 as low-end life ring. The eyes are exposed, and they lead to the same sinus cavity as the nose. I would think a full-face shield would be required atop the N95 to have any hope of true protection.

But your idea has more merit than you give it.

I used full-face, positive-pressure suits in nuclear power plants. As an operator we had to go places no one else was allowed or could, and watch our rad dose while watching out for physical contamination. I cannot remember the number of times we had to make up a set of hip waders out of plastic decon bags to get past unexpected water leaks in a situation where we didn’t have time to call for full body protective suits. And I lost exactly 1 pair of shoes to contamination, despite being at one of the dirtiest plants in the country at the time.

I also am familiar with those 3M dual filter respirators you are using at work, and I’d see those and a pair of soft-edged full goggles as a fair “emergency” PPE. Both could be deconed. Reducing the airflow around the eyes by having the goggles in contact would reduce the chance of droplets getting into the eye unless you were literally doused by ejecta.

Didn’t someone come up with a “smoke escape mask” after 9/11 that was in effect your plastic bag with filters. We need to check the filters cartridges and see of we can increase the protection factor, and you have your tin foil hat.

If it is big enough you could even fit one of those 2-cup holder drinking baseball caps in it (ok, that was meant as LOL material, but the smoke mask is honest).

I’m going to crank up Google and do a little search and report back. This is a time to borrow technology like there is no tomorrow - because if we don’t do something there may not be for millions.

NJ Preppie, I like the white one, always wanted to be an astronaut.

I told Kay she would probably die anyway as she is only 5’2”. Hey, maybe those Abe Lincoln stovepipe hats will come back in fashion for short people. Or those stupid hat umbrellas with a fan. Then you only need the bag.

But – would it work?? Something similar might allow the average Joe to go to work. If the kids can look retarded with their reversed ball caps, I guess I could wear a bag over my head. I know all this is silly but there really is a point to it all.

LOL JoeW - You’re terrific!!!

Guys and gals, Google “smoke escape mask” and look for several hundred hits. I think we are on to something! Costs are as low as $48 US smoke/toxins rated, $78 UD BIO on the first 3 I looked at. Man, I wish I had that patent!

Joe W. In principle it will probably work.

A side benefit will be that every one will give you a wide berth… you’ll have the ‘social distancing’ thing down pat.

Joe- open up the pdf description under biological suits. On page 8 is a half hood item. “Plyflow respiratory hood” It has full round clear head coverage, looks easy to wear. There’s a hole at the top and it has a fan and filter, that runs on a battery. How much could it costs, or maybe you can duplicate it.

So that leaves two questions.

1) Why is the index case infectious and the later cases don’t appear to be…could it be that the index case is infectious through respiratory droplets and the rest aren’t, while continuing to be infectious in body fluids?

 This is the reverse of what you would think or at least all cases would have equal infectivity.

2) The ‘IF’ question is answered…The ‘How Big’ question is answered…The only question left is ‘When’ and we should be narrowing the variables enough to make a reasonably accurate prediction.

Here is another way, might even send this one to Asia. Chinese people wear a conical hat. I am sure it has some name I just do not know it. Make a band (leather is used in western hats) to fit around the person’s head. Use the wire from a coat hanger to make a standoff and place the conical hat on the wire screen. We found that some sort of battery-operated fan is needed in the hat or it warms up too quickly. Place a hole in the conical hat, fill with cotton and cover the rig with a clear plastic bag tucked in the shirt. Of course you need a hole in the bag to breathe – I knew that
Even NJ Preppie would look stylish and might wear it in the Easter Parade.

Monotreme. I just re-read all the posts from my post at 16:32.

If you re-read my post at 16:32, I think there is the basis of an argument for your mammalian host other than poultry, which the virus shouldn’t be quite as well adapted…but for some reason is better adapted to humans post the index case…just a thought…

NJ Preppie thanks for the reference. I had a friend who used to get upset when they came up with an idea and then found that it was already in production. Seems to me that when you re-invent the wheel it only says it must have been a good idea. At least it was good enough for someone to manufacture it. Soo that is way cool. It works. Now to get the price down to under $1.99.

Sorry Tom if I hijacked the thread. I will shut up and listen now.

JoeW. There is no such thing as hijacking one of our threads. We are multiple-taskers in cyberspace…just don’t ask my wife to comment!!

Tom, I’m not so sure it would be the droplets decreasing in later infections, but that the strain is not as “wild” after a couple of human mutations. It still needs to zero in on the best point of transmissibility, and there has not yet been enough spread to get past a few specific binding affinities in familial clusters.

When it can hold on to make a couple of cross-family jumps, perhaps a cross-racial jumps, it will loose the specificity and become tremendously more virulent, and transmissible.

It may just be a snip of DNA, but for all practical purposes, it is like a macro-organism colony that is “learning” as it goes along - by environment, natural selection, mutation, recombination, etc. I think Monotreme is right about the last in the chain being the most dangerous, but so far we have seen the clusters die either because hosts became unavailable by death or isolation.

If the jump comes in a semi-isolated area (like a refugee center) during a long duration event with little available surveillance due to extreme conditions (like a volcanic ash fall keeping aid from getting through) for 3 infection cycles, then the odds favor the virus surviving - loosing enough specificity to more easier jump out of a family cluster to a general population.

In other words, what both Tom and Monotreme have me thinking is we are about at the end of the fuse on Java, and likely other locations that are not getting adequate surveillance. I don’t know how to give odds, but my gut doesn’t feel very good about this right now.

Hijack! What hijack? Can we go to the Caribbean?

maybe the virus just transmits better by coughing than by eating. The index case coughes and infects others. When those others start coughing they know that the index case has severe illness and other people are more careful, so the chain breaks.
So it would be the way how the index case coughes to others. Still not very effective and HCW usually avoid to breath in the virus while the patient is coughing. Also maybe it’s a special coughing and not everyone blows viruses with suitable droplets with a cough and not every cough is infecting others, only when everything is right from the virus’ point of view. However, this can be improved with mutations, maybe.
People rarely get it by bird contact but it’s possible.

Tray 75 There must be refugee camps in Indonesia now with the volcano / earthquake problems. Sure is reminiscent of 1918. You, Tom and Montreme’s conjectures tell us how it will happen. It would appear the stage is set.

Looked at the fire masks, if your engineer why not take the hat-mask and run with it. I bet if you could get it under $1.99 you could make a fortune.

I need to reload my coreldraw software and do a picture. Especially of the model with the double cup holder. We could call it the “Deluxe with Survival Tonic” and charge $10 at the flea market next weekend! You know, when it gets too heavy in here, the definition of enlightenment is to lighten up!

I got the place, the flea market in Rogers, Ohio is huge (one of the largest in the country) and it is about 10 miles from me. We get some of the most interesting people. Course you would have to allow for moodshine in at least one of those cups.

Been using CorelDraw since it came out — great package. Might even have a sprite with an unbrella hat. Now couldn’t you see that dance across your screen.

All-The main key that hasn’t been given out is could there be two differenct incubation times based on similiar viruses? That’s why when you lay out the facts we do have on incubation it doesn’t seem to make sense, and so WHO keeps enlarging it. I might be crazy but with case workers in the field the incubation time should at least be nailed down by now and the mystery should just be in the sequences. We are certain it’s just influenza right? Not influenza with a jolt of something else?

Hi everyone. Good points. It seems this virus is a wrong way corregan, the problem is it is very successful at going the wrong way.

It’s supposed to be a bird virus, to only adapt to other species once in a hundred years, yet this virus in a short period of time has adapted to several animal species.

It wasn’t supposed to kill aquatic birds and then later it was supposed to kill them before they could fly.

It wasn’t supposed to be asymptomatic in birds but it is not only doing that but it appears to be asymptomatic in pigs and probably other species as well…cats?.

It is definitely spreading more efficiently H-H than B or other animal to H.

Then index case is more infectious than the later cases with more viral passages…and there are other examples I am missing at the moment.

I’m not sure that the later cases are treated differently because in the areas that the infections are occuring, citizens aren’t well informed plus there were some escapes from hospital and family members escaping to other family to avoid hospital.

I’m not quite sure at this point what would explain it. However, it is probably another example of intermediate adaption.

Monotreme. You stated earlier that the way to acclimatize a virus to a new host experimentally is through repeated passages. Could you be a bit more specific? How many and what type of passages are we talking about? What is the success rate…How easy is it to do it and what kind of viruses have been successfully handled in this way?

Thanks.

Leo, you may just have hit on something there. Maybe in aerosol form the incubation is 2–5 and in fecal-oral it requires a longer time to “build up” and migrate to the lungs to show symptoms enough to get someone to seek care. 7 days+

Leo7 One thing about the sequences that bothers me is…do they have the basic knowledge to identify all sequences in this strains that would explain increased transmissibility or decreased virulence or signs it is loosing virulence all together or signs it is adapting to humans…

…I’ve got a feeling that even the specialists don’t know a lot about how to identify and correlate mutations with expression.

TreasureIslandGal. Good point. They may not have a lot of information on H5N1 but they should have data on other influenza viruses that could be applicable here.

If someone sneezes or coughs on me with a cold, it seems like I get the cold in a few hours. I would think respiratory spread with influenza would result in clinical signs quite quickly…ie. 24 hours.

As you noted, we should see a difference with fecal oral but I would still expect well below 5 days for incubation.

I think the wild extrapolations on incubation by the WHO was expedient…in other words, the least line of resistance.

Joe W - Now I did it. I can’t find Corel, so I tried editing in PowerPoint and here it is - the prototype SIP “SIPPER Deluxe” Emergency PPE Unit, Retail Priced at $9.99 for a limited time - batteries sold seperately.

Now, for real, these emergency bio-masks have some SIP potential, so I think some real investigation is in order. At this point, nothing is unrealistic if it works.

Tom DVM, I’m not a virologist, so take what I say with a grain of salt, but I think most viruses can be adapted to new hosts by passaging them. Certainly this is true of influenza. It is releatively easy to get a virus to adapt to cells in culture by putting virus on cells, waiting, collecting newly produced virus and then putting on the same type of cells again. Each time you collect new virus and transfer new cells, it’s one passage. This is very routine virology. Here’s one example with H3N2 cells: Reference. Virus can also be passaged by going from host to host. H2H is one passage. H2H2H is two passages. Here’s a short explanation in Wikipedia. The million dollar question is how many passages before the virus is fully adapted? That I don’t know. The fact that it is already virulent in humans indicates that it’s close. Now why that is never mentioned is puzzling. Every virologist knows this. Do any real virologists work at the WHO or the CDC? Sometimes I wonder.

Monotreme. It is entirely concievable that no virologists work in either agency. The thing is there is no special qualification to be a virologist. Aren’t you just as much a virologist as the next person. I think you said you have worked directly with viruses.

So many virions… So many hosts…. So many opportunities…

Just wondering, more the mechanical side of my brain on this, but have we ever before been able to so closely examine a true new influenza virus so early in its progression? This may be more the “prototype” from which the “manufacturing errors” are being worked out in rapid sequence by natural selection. Thirty years ago a girlfriend of mine was studying genetic engineering and for all the ways we discussed it, a virus is just a bio-chemical machine to make more machines, so forgive me if I don’t do the biology side of this as well as the mechanical.

So given a mechanism to mutate, by exposure to different animal hosts, it seems likely there would be successes and failures pretty rapidly in each new host species. Some birds die, some don’t, the virus that survive the longest in a host have longer to mutate by random changes, so that the next infection may not have the same environmental factors (the ambient air temperature or humidity is out of the envelope, too much sunlight, too much Tamiflu, etc.) to do as well as the index case. But as the generations pass, the sheer adaptability of the virus should find a way to overcome almost all the environmental factors, leaving only genetic sequencing to fine tune to a pandemic strain.

So could it be the clusters die out because the hosts change environments before the final generation can get itself together? If so, we could draw this out for years and still get a pandemic form of H5N1 just by it finally finding the right combination of host and environment, even though it seems to be “resting”? Would that match Indonesian, African, Vietnamese, and Turkish clusters scenarios.

Tom DVM, I have worked with viruses, but I am not a virologist. I used them as a tool. For me, they are were a means to an end. But I do know some real virologists and they are very serious preppers. H5N1 scares the bejeezus out of them.

Tom DVM, I have worked with viruses, but I am not a virologist. I used them as a tool. For me, they are were a means to an end. But I do know some real virologists and they are very serious preppers. H5N1 scares the bejeezus out of them.

Monotreme. What makes one a virologist…field of study?

take a diver’s glasses equipment with snorkel. You can even make the snorkel longer by attaching some plastic-tube to it and maybe put some nanofilter into the tube. You are breathing “upper” air, the “mask” fits well (waterproof) and there is a good filter far away from your nose. You can add another filter, in case viruses are trapped in the first one and that one becomes leaking. There could be small filter-tubes of several sorts which you just plug between the snorkel and the plastic-tube.

Many Cats, you probably already have seen this page, but for those who haven’t, here’s the list of animals shown to be infected by H5N1.

TRay75, I think it is true that you need both the right environment and the right mutations. I think we are very close to having all the right mutations. Many people are concerned about the upcoming flu season in the Northern Hemisphere, but it’s flu season even in the summer in Southeast Asia.

TRay. Here’s how I see it. The index case is a super-shedder or a very efficient spreader and this must be in respiratory droplets. The person must be infectious, by this mode of action, for a relatively short period of time. Therefore, the only persons who would contact the person at this time would be family members. Community doesn’t get it because the person is not infectious in the early stages…Healthcare workers don’t get it because the person is not infectious in the later stages.

The problem then becomes what is going on with the secondary and tertiary cases. You would think that they would be as infectious as the index case and therefore they would repeat the pattern and maybe start infecting community members and hospital workers.

That’s the one we don’t have an answer for yet…it sure is funny.

By the way, when someone starts seriously discussing specific mutations…I start to drift off in a hurry…just can’t get my head around it for some reason.

Ugh, FluWiki ate one of my long posts after it appeared. Oh well.

I strongly recommend this paper.

Click on it before it disappears!

Tom DVM, a virologist is someone who tries to figure out how viruses work, which is not me, except as a hobby :-)

Earl Brown at the University of Ottawa is a real virologist. He’s also the first author of the paper I cite above.

Monotreme: Not that I ever have anything valuable to say, but if you highlight your work and right-click and copy it before you post, then you only have to paste back in if the Wiki Gods are in a wrathful mood. I have saved myself some agitation with that after a few losses… :)

Many Cats, I always copy my post before I save, but tonight the Wiki gods are wrathful. I saw my post up for several minutes and several posts after it. “‘Then’‘ it disappeared leaving other posts intact. I had saved latter posts by then. I should have created a page of posts and checked back after a good half hour. C’es l’vie.

Wow! It just ate Tom DVM’s post, too…..

by the time there are tertiary cases, people know that the primary case had bird flu and are more cautious.

Hi all. I just had two post in a row eaten. Oh well, maybe I should take it as a sign.

I’ll try one last time. Monotreme. Studying viruses as a hobby makes you a virologist. I think I will make myself one cause it sound goooood!!

Is the paper the same as you lost earlier. If it is could you give a summary for those of us who drift off as soon as descriptions start on specific mutations. Thanks.

Maybe one of you guys could start a new thread, part III. Just in case the lenght of this one is causing problems. I would try, but I haven’t conquored the tinyurl thing yet and would not be able to harken back to this thread without causing the evil sidescroll…

We are back in the perilous waters of under-capacity and over-usage.

Tom DVM, I’ll try to summarize the paper I mention above and what I think the current status of the virus is either tomorrow or Thursday. Flu Wiki is wrathful tonight.

Many Cats.

I read every postof yours that I see.

Second, thanks for the advice. I am computer illiterate and have great difficulty reworking lost posts.

Monotreme. Thanks!!

I unfortunately don’t share your great interest in the intricacies of mutations.

One thing I noticed on the CNN newsreel was that the infectious recovery ward was open to air, but I’m sure the critical area isn’t. Open air may be helpful for preventing HCW’s from contacting virus from work surfaces etc. The second and third level exposure cases are puzzling to me as well. I’m thinking a shared water source, bucket and dipper etc, but surely WHO would’ve tested that out. When a virologist is worried, I’m worried.

Tom, I get what you mean about wrapping your head around this. I was glancing over the link that Monotreme just sent and a thought went trough my mind as read about the changes in virulence in mouse generations on the tests that were being run. If a virus spreads by rupturing the cell membrane wall, not all the Virus will be expelled, just those that can hitch a ride on exhaled H2O, phlegm, etc. Could the nature of the medium change as the infection escallates, such that less of a certain secretion is present as the temperature increases or the dehydration in the tissue around the infection increases. Again, this is an environmental / mechanical though, not bio-chemical. That would account for a window of “super spreader” capacity as the illness progresses. You could become so sick that you could not spread the virus after a certain point because it doesn’t have the travel medium to hich a ride on. We know that the firus seems to be adapting to lower temperature media for infection. That could be the tweak, it hasn’t become broadbased enough to spread if the hydration or temperature is out of parameters. So if it continues to work in a host, it kills them with a limited window of spread, but during that window it is deadly contagious. That could be better at containment than carpet bombing Tamiflu (personal openion, we used the medication too soon, and by the time it does break the close environmental bounds it may also have considerable Tamiflu resistance, so we shot our big gun before the real war even started). Monotreme, I know it is a hobby, but can organisms be so environmentally restricted as to have a limited window to hitch a ride out of the lungs? I’m learning so fast today my hair hurts, what little there is left of it.

anonymous - at 23:53

Noooooooooo! Some of us might not comment very often, but we are here reading. gina

Tom DVM: You are always a gentleman! Unfortunately, we ancients have to catch up with all the subtlties of internet/computer life. If you go to the news thread, they had a side discussion of “mouse over”. We keep learning out of necessity. I just hope we learn enough to keep as many people safe from this potential cataclysm.

TRay. I don’t see why not…it could very well be something like that but I stick to expression and try not to delve to deep because I just confuse myself…but you go ahead…its interesting to read.

One thing you said…”We know that the firus seems to be adapting to lower temperature media for infection.” I’m not sure exactly what you mean by this but the virus at its starting point in poultry was only viable at higher body temperatures, outside that of humans…supposedly.

Wiki is definitely having problems, I see one of my earlier posts disappeared about a new detection device that was there before my last post.

But, it is midnight, and I need some sleep while I can get it. Let’s see what the ‘morrow shall bring.

I appreciate the exchange today. It feels good to be able to ask questions and learn from others and fell like I have something to contribute. Honestly, it’s been a really crappy week to date, and it isn’t looking better tomorrow.

I guess the Wiki gods ate the end of my sentence: ….as possible. :(

Tom, that was exactly what I meant, it is able to thrive a lower body temp and it is closing on our upper respiratory range.

anonymous at 23:50. I agree with what you generally speaking, but the period of shedding would be earlier that they would present to a hospital and the community in this area did not seem well informed. Also we have had patients escaping to other family members and escaping hospital at a point when they may have been in the short contagious period.

Could the decrease in the spread of the virus be due to the amount of damage to the lungs? gina

Monotreme at 23.31 Good article and scary as well. I think the next time I get angry instead of saying I’m feeling postal;I’m gonna warn I’m feeling viral.

Gina. Entirely possible.

I’ve seen how fast a virus like this can destroy lungs…it’s a scary thing to watch.

Why don’t you take a shot at figuring out the problem in the second paragraph of my post at 23:31…it is really bugging me!!

By the way, I read your comments when I see them too!!

Tom. My thoughts and they kind of link into your post at 23:31.

The index case has a strong productive cough in the initial stages, because the virus has just started to damage the lungs. This is the critical stage of transmission. At this point, it would seem proxcimity would be a key factor in the spread of this virus Howerever, as the virus moves rapidly through the lungs causing extreme damage as it goes, the lungs are unable to rid itself of the virus due to the hosts weakened state. Reduced or no cough. Reduction in contagion. As far as other cases in the family… those with the stronger cough reflex would be able to move the virus through air droplet than those with a weaker cough reflex. Right now, as long as the virus is in the lower lobes of the lungs it will have difficulty spreading. When it decides to migrate to the upper lobes is when TSHTF. There will be no stopping it. In all actuallity, this virus only has one mutation left. This virus IMHO is very smart and mankind is it’s altimate target. And we think we are smart. gina

Tom, but you won’t spend a night near a person with birdlu coughing and escaped from a hospital. Once the index case dies, people will become cautious. That leaves the question, why the 2nd case in a cluster is so often a family member. We should compare this with normal flu or other infectious diseases. Is there some data ? Ask some people in birdflu-regions who had had normal flu, whether they did infect other people and whether these were family members.

HurricaneAlleyRN,sounds reasonble to me, except the one mutation and that the virus isn’t smart. When the virus is in the lungs, then it won’t be coughed out ? What can make it go upstairs ? Is it just these alpha 2,3 cells which are needed ? At least it seems that this feared asymptomatic infection plays no role actually.

New thread

Thanks, Monotreme. :-)