Dr Taubenberger’s post on 1918 virus
This forum is a continuation of the the excellent discussion begun by Monotreme on 18 March 2006 H5N1 Evolving Towards Pandemic Strain.
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Origin and evolution of the 1918 “Spanish” influenza
You have to elaborate on that last post. Are you suggesting that because there was no smoking gun, the sequence must be incorrect?
AA-
Not at all. I am only addressing the issue of what is unknown.
If we can’t even pinpoint a sequence portion that is tied to virulence in the 1918 frankenvirus, then perhaps we don’t have the correct sequence or perhaps we are seeing widely diverse characterisations / expressions that we don’t understand.
I do wonder if we’ve missed something due to experiment construction? But I’m not stating with any certainty that we’ve missed something. Just thinking about it.
There’s much more work to be done, so I think that we should stop crediting causality and positive knowledge to material that is still very much under development.
Alright I just read your last post in the original thread (sorry about that again).
You are mistaken that the sequence posted is some sort of “average.” That sequence in the figure is the sequence from the S.C. case. That’s it. No “averageing.” No guesswork. That is the sequence. You will notice that where the other two cases differed, they noted it.
NS: I guess you do have a point. The virus that wiped out an Alaskan village in 1918 could have been something else. But I doubt it.
aa-
I don’t contend that teller mission was visited by anything other than what Johan Hultin excised.
I do wonder why we continue to compare H5N1 with PF11 in 1918 when we have so little complete info on the 1918 isolates and with what we do have, we must speculate tremendously to pattern match to H5N1.
AA-
You’ve certainly followed this work very closely and expertly.
Did you work on or with the J.Tau team doing the sequencing, by chance?
Were the primers optimal or were they based on some very strong guiding assumptions?
Is there any possibility that we could be looking at different chains of nucleotides under different laboratory procedures?
The 1999 paper cited at the top has been updated a tad in terms of the knowledge base over the last 7 years, though the point remains (and one I’ve also made): 1918 H1N1 and 2006 H5N1 are, in their own ways, unique, including in comparing them to each other.
aa, thanks for sticking around and contributing. Your insights are appreciated. NS1, gret contributions to the wiki.
And I’m glad you started a new thread. ;-)
I was going to say exactly that, Dem!
NS1, you are quoting a very old paper from a time when Taubenberger’s project to sequence the 1918 virus was incomplete. You might want to be more up to date before giving your opinion about what is unknown or specify that it is only unknown to yourself.
The following excerpt is from Characterization of the 1918 influenza virus polymerase genes Nature 437, 889-893 (6 October 2005)
“RNA isolation, amplification and sequencing. RNA was isolated from frozen 1918 human lung tissue using Trizol (Invitrogen) according to the manufacturer’s instructions. Each fragment was reverse transcribed, amplified, and sequenced at least twice. Reverse transcription polymerase chain reaction (RT–PCR), solation of products and sequencing have been previously described4. Lists of primers and primer sequences are available upon request. Replicate RT–PCR reactions from independently produced RNA preparations gave identical sequence results. The 2,280- nucleotide complete coding sequence of PB2 was amplified in 33 overlapping fragments. The 2,274-nucleotide coding sequence of PB1 was amplified in 33 overlapping fragments. The 2,151-nucleotide coding sequence of PA was amplified in 32 overlapping fragments. The PCR products ranged in size from 77–138 bp.”
Just to add to the last post: the fragments were not all from one subject. Over a number of years, there had been various fragments collected. The Alaskan one was the one that gave the richest results as well as finally linking all the fragments together. Fragments from this one source also provided confirmation of some of the previous sequences.
No, this is not guesswork. They HAVE CORRECTLY gotten the full sequence of the 1918 virus. They may not have the full physical sample of the complete virus from 1918, but the information from the virus sequence is all available.
NS1,
“If we can’t even pinpoint a sequence portion that is tied to virulence in the 1918 frankenvirus, then perhaps we don’t have the correct sequence or perhaps we are seeing widely diverse characterisations / expressions that we don’t understand.”
For a description of the characteristisations of the 1918 virus and what can or cannot be deduced from what we know, read the article from Nature October 2005 that I quoted above. It also contains an interesting discussion as to why Taubenberger thinks it is likely that “the donor source of the 1918 virus was in evolutionary isolation from those avian influenza viruses currently represented in the databases.”
“I do wonder why we continue to compare H5N1 with PF11 in 1918 when we have so little complete info on the 1918 isolates and with what we do have, we must speculate tremendously to pattern match to H5N1.”
We continue to compare H5N1 with the 1918 virus (I refuse to use your nomenclature if you don’t mind) because there are numerous features that are common to these two that are NOT common to other avian viruses that do not cause human disease. I am only going to quote one example otherwise I will have to reproduce the entire article:
“Perhaps most interestingly, the 1918 virus and subsequent human isolates have a Lys residue at position 627. This residue has been implicated in host adaptation, and has previously been shown to be crucial for high pathogenicity in mice infected with the 1997 H5N1 virus. Of the avian isolates, 19 out of 345 have a Lys residue at position 627, 18 of which are HPAI H5N1 or H7N7 avian influenza viruses. Sixteen of these were recently characterized H5N1 isolates from a die-off of wild waterfowl around Qinghai Lake in western China in 2005 (ref. 21). In human H5N1 isolates, 11 out of 37 have the E627K change: A/Hong Kong/483/1997 and A/Hong Kong/485/1997, four out of six isolates from Vietnam in 2004 (ref. 22), and two out of three isolates from Thailand in 2004 (ref. 23). The E627K mutation was seen in six out of seven H5N1 isolates from Thai tigers in 2004, and was also present in the H7N7 virus responsible for the single human fatality during the HPAI H7N7 outbreak in the Netherlands in 2003 (ref. 20). It was not noted in the contemporaneous chicken isolates.”
I assume, this is the PB2-gene. So, chicken have E627 - then it infects humans and often mutates to 627K inside the human ? Or most chicken viruses are E627 but some few are 627K and these are much more likely to infect humans ? I assume the first infection in the lungs by breathing is different from the infection with subsequent copy-virus-releases generated in the human. Maybe only the first kind or only the 2nd kind of infection prefers 627K. Looks, that E627K is also a bird mutation which happened in Qinghai and not only a human mutation
Anon and Friends-
I am working from the information in that old paper because it was presented as the basis of the topic raised earlier. We are all aware that more recent publication exists. That being said, time passage does not always equate to progress.
There are some similarities geneticially for H5N1 de jure and the frankenvirus built from the 1918 fragments. There are more glaring differences though. If we continue to make prima facie exactions on the two, we are performing a dis-service to those seeking full understanding.
The Lysine acquisition at residue 627 on PB2 is found in all commonly circulating human flu strains.
anon-
Is a fragment a fragment or is a fragment called something else? Does the number 1 as in “complete genomic sequence of 1 virus” mean something other than the number 1?
1918 Influenza, the Mother of all Pandemics
I only contend that we should properly define these things for what they are … RT-PCR from fragments that are used to verify other fragments with only 1 completion of the full 8 required gene segments.
None of these studies took place with a viable sample.
Is this a true statement? If not, please provide more information on the live virus that was isolated, allowed to replicate and sequenced from PF11 in 1918? I’d be very happy to have more conclusive evidence.
Again, I ask, is it possible a different protocol, variant experiment constructions or updated base assumptions may drive us to a different outcome in the final sequencing? If we had enough tissue material to continue our probing?
NS1
Again, I ask, is it possible a different protocol, variant experiment constructions or updated base assumptions may drive us to a different outcome in the final sequencing? If we had enough tissue material to continue our probing?
That’s a great question to ask Palese or Taubenberger. It’s expected, depending on where the probe is looking, that there’d be variants, although these original samples were from a killer strain, given who they were obtained from. But would minor variants change the Big Picture, let’s say, for HA?
Is this a true statement? If not, please provide more information on the live virus that was isolated, allowed to replicate and sequenced from PF11 in 1918? I’d be very happy to have more conclusive evidence.
But you can tone down the outrage, and simply make your point. You’re amongst friends. Or you’ll wind up arguing with yourself. ;-)
In the end, 1918 provides insight, not proof.
NS1,
I think you misunderstand my point. I am not arguing whether it was one particular virus or multiple strains of the virus, because any pandemic could involve multiple strains. Rather, I am trying to point out that your previous posts create the impression that our knowledge of the 1918 virus is a lot of guesswork. I am saying it isn’t.
What I am trying to point out to other people reading this thread is that the sequencing was not guessing. Perhaps the easier way to understand what Taubenberger and his team had done is to use the analogy of puzzles sold at games stores. Now if you are putting together a regular puzzle which is created by cutting up a picture, how would you know that a particular piece that you are holding has to belong to that particular position and not anywhere else? What are the clues? The clues would be the precise shape of the interlocking edge and the fact that when you put the piece in, features of the original picture which were cut up before now align perfectly, such that if you have done every piece correctly, it forms a congruent picture and not a jumbled-up mess. If the original was a picture of a person, for example, your finished product would perhaps let you recognize that person.
The fragments that they worked with were basically long strings of code. Because these were not obtained from one single source, (and here the analogy to the puzzle does not apply) the sequences at two ends of each piece had overlaps with other pieces. (There would have been strings with no overlap which would not give you any clue as to where it should go and were therefore useless.) These overlaps serve the same function as the unique shape of the interlocking edge in a regular puzzle - they allow you to know where that string should go in the whole sequence.
In any scientific endeavour, there is going to be a margin of error or confidence limit. In this instance, the longer the overlapping segments, the more confidence you have that this is correct. (Quantitatively, there must be a statistically significant number for that confidence which other more clued up can give.) This is the same as when you put together a puzzle. One can always argue that unless you were physically present and observe how the puzzle was cut up, the fact that you have regenerated the picture does not prove that you have obtained the original picture. And of course you have not obtained the original picture. All you have done is re-created a recognizable facsimile that has enough details from the original to give you a lot of useful information. Just as putting together the picture of the person allows you to recognize that person and use that information.
Science is only as useful as what we make of it. The most important contribution of Taubenberger’s work is to create a model for our understanding of what happened in 1918, and to provide a framework for subsequent researchers to embellish in our desire to seek knowledge about current viruses.
In addition, mainstream research requires rigorous protocols which go through peer reviews and reproduction by other researchers. Let me point out that others far more eminent than myself like Robert Webster and Arnold Monto and Albert Osterhaus and so one have fully accepted Taubenberger’s findings and conclusions.
It would also be very odd (and perhaps the height of double standards?) especially for those folks on this forum who cheerfully accept Niman’s propositions everyday and consider this as not satisfactorily proven.
gs,
You have picked up on a very important point.
“So, chicken have E627 - then it infects humans and often mutates to 627K inside the human ? Or most chicken viruses are E627 but some few are 627K and these are much more likely to infect humans ?”
For the Thai tigers and the H7N7 cases, the mutation was not found in chickens at all. It is theoretically possible that some of the chicken viruses are 627K but not isolated, but it is more likely that in these cases the virus mutated within the human or tigers. But we don’t know for sure, because we know from Qinghai that the virus can mutate in wild avian species.
“Looks, that E627K is also a bird mutation which happened in Qinghai and not only a human mutation.”
Yes, but interestingly 18 out of the 19 found were in HPAI of H5N1 or H7N7. And 16 out of these 18 were from the Qinghai die-off. This puts into perspective the importance of this particular mutation that happened in Qinghai.
Immunologists, please answer this question. It seems reasonable to me to go ahead and make a vaccine for the current H5N1 even though it probably will not provide direct protection. My reasoning is that at least our bodies will have some exposure to this virus type and perhaps will not overreact when avian flu goes pandemic. Giving a vaccine now may provide indirect protection. Your thoughts??
CC:it depends on how much the vaccine costs. Anyone knows ? anon22:how do we know that the mutation occurred in humans ? A lot of bird- viruses might have entered the body and one of those few with 627K might have succeeded to enter a cell, while most of the others had failed ?
What if an inefficient and untested vaccine is developed and given to healthcare workers who become asymptomatic ‘shedders’ of H5N1?
anon22,OK- reading your post again, you already said, it’s unlikely. Would be interesting to know, how many viruses you get usually - the media here say, you need lots of H5N1 currently. Why is it ? One would be sufficient or not ? Except if only some few mutants are capable of entering cells and these are unlikely in small loads. Also, how many generations of viruses happen during one illness ? Hmm, H5N1 is almost always a severe disease whether with or without E627K. So the virus does enter cells. But then why should there be an elective advantage of 627K as long as it doesn’t jump h2h ?
Tom DVM – at 13:06
Tom, what if the vaccine had been tested (hasn’t the current vaccine been tested already?) and the government ramped up production for everyone. So in a year or less every single American were vaccinated wouldn’t that eliminate the worst case scenario?
BP. The testing of current attempts has not been very good. The immunologic response was rather poor and proof of an immunologic response should not be confused with proof of effectiveness against viral challenge. I believe I read that in 5 years, with current technologies, they would have capacity for 200 million people if the antigen required was equal to that used for seasonal flu’s.
As I have said before, the virus and its infective characteristics (phenotype) that we are seeing today may be rather remote to the characteristics of the final version that may have several other mutations, possibly lowering the effectiveness of any current vaccine.
According to the WHO, current global manufacturing capacity (of regular trivalent influenza vaccine is estimated at 300 million doses per year. Before we even get into the higher doses required to render the experimental vaccines effective, we’re already talking about multiplying manyfacturing capacity by more than eighteen times what it is now.
Thanks Racter
CC,
“It seems reasonable to me to go ahead and make a vaccine for the current H5N1 even though it probably will not provide direct protection. My reasoning is that at least our bodies will have some exposure to this virus type and perhaps will not overreact when avian flu goes pandemic.”
You are exactly right. Various vaccine companies ARE working on making vaccines, using seed strains currently available. In fact, the US government has recently authorized plans for a second vaccine. The first one was made used a strain from Vietnam from 2004 (what we call the ‘Clade 1′ virus) before the more serious outbreaks in Indonesia and subsequent outbreaks spreading to Europe and Africa. The new vaccine will use the Indonesian Clade 2 strain from 2005.
CIDRAP reports on this on March 6th.
Exactly how these vaccines will be used is still undecided. It would presumably be useful for first responders as a primer, so that when a pandemic strain actually appears, they only need one booster dose of the pandemic strain rather than having to wait for 2 spread over several weeks.
how much of that vaccine will they have, who will get it, what will it cost, what’s the probability that it will work ?
Anon22 at 09:31
No time to read the remaining posts after the response at 09:31. Will contemplate those later today.
I agree that J.Tau and Co. did an unimaginable feat in going from fragments to frankenvirus and that because of their ongoing work, we now have the palette of science on which to paint our art of epidemiology for PF11.
Just a few immediate thoughts about the puzzle . . .
The puzzle metaphor is a stretch for the 1918 work, but a very nice one.
Why do I say that?
Perhaps we should extend your metaphor.
We have 3,432 pieces and the top of the box is missing, the one with the final or target picture. We do locate a small paper insert that has a description of the puzzle, New England Lighthouse c. 1918, a puzzle in 1,000 pieces. This insert also has a black and white, small 2”x3” photo on it.
Apparently four copies of the puzzle were purchased some time ago to simultaneously stimulate four children and over time, the children have misplaced enough pieces that the parents have combined them all into the one box you are holding.
Increasingly suspect is the fact that you have pieces that do not seem to match the picture at all, a full white background, when there is none in your low resolution photo guide. But the white pieces DO fit into sections of your New England Lighthouse by shape and by shape only, so you hope that you just missed something in the matching picture and you hope that the white belongs because none of the other 3,431 pieces fit in that position by shape. Do you see how we can start reaching for conclusions when we sometimes don’t have the answers?
The probability exists that another puzzle, unrelated, but from the same manufacturer using the same cutting die to make the same shapes, has also been swept into your collection box that already contained portions of the 4 New England Lighthouse puzzles? Busy and overburdened parents at the end of a long evening after putting the children to bed often work with an end in mind rather than minding proper puzzle segregation technique.
You have fashioned a lovely straw horse, carried it into town, stood it at my market stall, gracefully mounted it and from atop your lovely stead, you’ve instructed me to feed him. I wistfully stare into your valiant stead’s walnut eyes for a moment, appreciating and admiring your effort and contemplating my acceptance of your argument. Then, I cheerfully pluck a few strands from behind your creation’s ear and, with a nod of indifference, offer it into the straw horse’s mouth, making the chewing sounds myself.
DemFromCT – at 07:38
You are exactly on mark with the statement that 1918 provides insight, not proof.
I’m working here to maintain the facts in one corner and the suppositions in the other for all those readers who may be over-adequately awed by famous names and then miss the missing links.
No outrage intended.
Note the civility in my request for more information.
Righteous indignation at anon22 for his pedantic pitches and ad hominems, oh yes, but not outrage.
Outrage creates rebuttal with dissonance, something we see often here, but a tactic that is ineffably inefficient if we wish to Gather and Solve.
NS1,
The puzzle metaphor was used for illustrative purposes for those who find discussions of sequences a little too esoteric. It is not supposed to be a representative model for a discussion of viral sequences.
:-)
The 1918 influenza virus was sequenced just like all other influenza viruses, namely by reverse transcriptase-polymerase chain reaction (RT-PCR). RNA was isolated from the tissue, reverse-transcribed into cDNA and then PCR amplified with influenza primers specific for the fragment in question. The only difference between sequencing 1918 and a modern virus is the SIZE of the PCR products. Modern viruses, for example, can be amplified and sequenced using primers 1000 bases apart but RNA quality in the 1918 material required amplicons less than 100 bases. The puzzle analogy doesn’t work.
In fact the quality of sequence in the 1918 cases is generally much higher than the average flu sequence in GenBank for two reasons: 1) each base was confirmed by sequence in each direction and in multiple independent reads from several independent RNA isolates, and 2) because it was determined directly out the lung with no lab adaptation sequence artifacts like one sees when a human virus is cultured in eggs. The complete 1918 virus was sequenced from one case and partial sequence was determined for several other cases. Variations between cases were reported.
That the 1918 virus does not possess known mutations already associated with increased virulence in other influenza viruses does not mean that the sequence is incorrect, rather that our understanding of the relationship between viral sequence and the pathophysiology induced by it in particular hosts (genotype-phenotype correlation) is still very primitive. Animal models have already demonstrated the importance of the 1918 HA and NA genes for mouse virulence and polymerase function is likely to play a key role as well. On-going work is attempting to map specific amino acid changes in these proteins with different phenotypes in various animal and cell culture experiments.
This work will shed light on how influenza viruses cause disease and will have relevance for understanding H5N1 if parallel molecular mechanisms are observed.
Made sense to me — thank you.
Dr. JKT-
I take a breath of fresh air in reading your response.
Your taking the time to visit and clarify is wholeheartedly appreciated by all.
Though it has been attributed to me by others, I do not suggest and have not at any time suggested that the 1918 sequences are incorrect. I have asked about potential varient outcomes under different assumptions and / or protocols.
We each are using the results of your in-depth and timely projects as a basis for our efforts. And in this matter, we do truly stand on the shoulders of giants.
I’m only asking for a plaintive consideration that our understanding of the 1918 strain(s) is still under development and that many of the prima facie presentations of parallelism to H5N1 may lack the extensive evidence typically required in matters of such grave bearing.
We wait and watch for further publications.
What is your current finding the the importance of residue 92 on gene segment 8 of H5N1?
Again, we are honored.
JKT-
Do you have work-in-progress factored around any unusual phenotypes or are you working within classical influenza models?
Do you give any creedence to the idea that some intrinsic growth factor expressing in concentration in certain human age groups, e.g. very young, young adult and pregnant women, may be correlated to the high virulence of the 1918 strain and / or the H5N1 of day?
Many of use are very interested in the continuation of your search for a first-wave 1918 sample as a virulence comparative?
Niman-
What is your current interpretation of the HA cleavage on the Indonesian vaccine strain? Do you feel that the A90T polymorphism is as significant as the S227N?
Did you expect this strain to be chosen for the vaccine?
Tom DVM – at 13:06
Can you detail any reports of asymptomatic shedding after an H5N1 vaccine? I’m very concerned about a “one size fits all” vaccine. There will exist certain members of any population who will have an entirely separate reaction to a vaccine than the majority.
What are the likely parameters for the post-vaccine asymptomatic shedding scenario to occur? Can you discuss this situation from personal research with other vaccines?
NS1,
The human vaccines being made for H5N1 are inactivated, i.e. killed so there is no problem with shedding. The only live vaccine for flu at the moment is FluMist, in the form of a nasal spray. I don’t believe anyone is working on making a H5 version of this.
Annon 22 and NSI. It is not a question of shedding an altered modified live H5N1 vaccine strain. As has been clearly demonstrated in China, vaccines with incomplete or inaccurate or misdirected immunological response, can result in animals being infected during a pandemic and then becoming asymptomatic shedders, spreading the disease to others. An immunologic response to a vaccine does not prove an effective immunologic response to viral challenge.
After 1997 when Dr. Webster and the Hong Kong authorities were supposed to have eradicated the disease, some believe evolutionary pressures were accentuated by the use of vaccines and antivirals feed directly to chickens in China. The disease smouldered and evolved secretly in China until it was discovered in border countries in 2003.
Tom,
I guess I got the wrong end of that question then :-)
However, if and when we are already in a pandemic scenario, I don’t suppose it would matter that much whether there are asymptomatic shedders walking around because they have been vaccinated, would it?? Because there will be plenty walking around shedding viruses because they have been infected…
The solution in poultry is for each batch to leave some (‘sentinel chickens’) unvaccinated so that we can observe/test them. The equivalent ‘sentinels’ in a human pandemic would be the large majority of people who will not have access to the vaccine for a long time.
EEEK!!… <rubbing off goose-bumps>
Annon 22. In my opinion, the best way to deal with H5N1 in chickens is to increase biosecurity and then allow the intermittent infections and immediately aggressively cull the birds.
In animals, with specifically and only influenza’s, it would be far better to use whole flocks as sentinels than to allow what has happened in the past…vaccination hides infections and allows a rapid expansion of viral passages through large numbers of domestic animals which equals more mutations etc.
I agree with your point about healthcare workers during a pandemic but this could potentially rapidly accelerate the early spread of disease…we may never know the answer.
Annon 22. Vaccination may suit the industry best but I am not sure it is the best strategy with flu’s for disease eradication.
Tom,
“In my opinion, the best way to deal with H5N1 in chickens is to increase biosecurity and then allow the intermittent infections and immediately aggressively cull the birds.”
Unfortunately, in most countries, the situation has moved beyond that. This would still be ideal for some European countries or the US.
Interesting article from a front line physician http://tinyurl.com/oytnn name of Dr J. Farrar who works in Ho Chi Minh City and has treated 24 (or so) pts with the bird flu. He talks about the spread and possible evolution among other things.
It just occurred to me, would the people who post on this thread consider contributing their demographics to the “Flu Wiki Survey, Please participate.” It could be helpful to the goals of FluWiki. Thanks for considering it. I lurk and learn on this thread.
This thread is quite interesting. Going forward, could there be a possibility of the middle eastern bird flu meeting with the Indonesian bird flu in Canada and producing a really bad virus?
Torange Influenza viruses are truely unique amongst pathogenic agents. It could jump at any time at any location in the world including North America, once infected birds reach here. If I was a betting person though, and I’m not, I would bet on either China and Indonesia or one of the closeted countries in East Asia. The virus has had longer to assimilate and adapt to humans there.
anon_22 at 09:16 - “The only live vaccine for flu at the moment is FluMist, in the form of a nasal spray. I don’t believe anyone is working on making a H5 version of this.”
MedImmune (maker of FluMist) is working on an H5 version: http://tinyurl.com/zl4ts
Anon22 and Tom-
Continued passage through vaccinated animals allows proximity and proximity creates opportunity for genetic acquisition as Tom has mentioned. Vaccination of animals appears to create a breeding ground, undetected primarily, for this virus. This low detection, smouldering effect, provides an ideal environment for co-infection and re-infection within a large flock. A very high number of permutations may be created in a short time.
As nightowl has added ‘live’ virus vaccination is being developed by MedImmune.
Even the attenuated vaccinations fail at times to fully attenuate because every batch is different and the formalin, formaldehyde or beta- propiolactone is held reasonably constant or the heat method is employed without success. Insufficent attenuation will leave infectious virus capable of insinuating disease. Live virus can be found in today’s vaccination stock.
I’ve seen specific examples of mid-term paralysis created by neuro-infection after an attenuated seasonal influenza vaccination in perfectly healthy, fit individuals. Watching one robust Big 10 college football player be rescued from death shortly after a “flu shot” and then spend 12 months in a wheelchair is eye-opening.
NS1-re: “I’ve seen specific examples of mid-term paralysis created by neuro-infection”
Is this something different than Gullian-Barre?
TOM DVM:
Do you have the ability in your own clinic to test any birds for H5N1?? Or do you need special equipment for that? There will be lots of babies soon, easy to handle - or even chickens??
there are influenza-A-quick tests for about 5$ per test. But I think for specifying H5 you need a more complicated test
I was wondering if perhaps Tom DVM has a buddy in the lab at Guelph (big vet school here in Ont) who cd test them - or perhaps we could pay for it? Just would be interesting to know if wild birds are carrying it. We have many Eastern Bluebird boxes on our property which will soon have bluebird or tree swallow babies which are easy to take from the next for a few minutes to extract fluid or poo sample and banding. Even if we only tested a couple of dozen - wd not be too expensive and the results might be fascinating!! Rather than wait for our SLOW govt to get around to it??
gharris. I’m sorry if I have inadvertently mislead you. I had my own practise for twenty years but am now on sabattical. I may go back at some point…I may not.
The authorities including the Ontario Veterinary College will probably be testing any bird presented to them this summer. In my opinion, it is not whether they will test, it is who controls the information on the tests. If anyone in Ontario finds a dead bird, I would call my MPP and ask them to tell you where to drop them off and the testing protocols that have been established. I have enjoyed your posts. Keep up the good work.
Thanx Tom DVM (blush!!)
the index said, there were a recent post of anon_22 in this thread, but I can’t find it
anon_22 put the Taubenberger anchor link at the very top. It goes directly to his post (for gs, who doesn’t like wading through long threads).
yes, JKT’s post to explain the reliability of the 1918-sequence and some vague future projects. Taubenberger is a very prominent member in the “no one knows” camp, I wished he would speculate/guesstimate a bit.
gs - welcome back to what IMHO is the very best, most interesting thread at the FW. I can’t wait for the discussions to start once again!
So happy to have this site up and running again. I really missed it. How about that article in the postbulletin about Dr. Gregory Poland. I believe the posting actually came from Fluwikie. I saw it this morning on flutrackers. Anyone want to comment about that?
Please see my post from a few minutes ago on main forum - I did not post a heading for it - should have been ‘Viral Peptides’ - I thought it might be important for one of you scientist types?? Anybody care to comment on it?? if not - cd one of the mods pls move/delete it or fix heading?
Older thread, closing for speed purposes.
check dates