Forum: Questions for Dr Taubenberger

Dr Taubenberger has kindly agreed to give an interview with myself for Fluwiki. I have a preliminary list of questions down. If you have questions that you would like to ask, please post them here. I suspect there will be far more than can be covered so most likely I will condense them into a manageable list. :-)

Hi Jeff, if you are reading this, thank you for helping us all understand influenza virology a lot more. The more we learn, the more question everyone has!

Here are some of my questions, they are as I said preliminary and not well constructed yet.

1. where do you think the 1918 virus came from?
2. what evidence do we have concerning this, why do we need to find out more and how would one do that?
3. do you still think that 1918 H1N1 and H5N1 are “kissing cousins”? Why? How are they different?
4. tell us about what you are working on?
5. you’ve found H3 in the pre-1918 patients. What is the significance of that, especially given the current circulating seasonal strain is also H3? Some people propose theories about how pandemic flu viruses are cyclical, do you think so and why?
6. There are 16HA and 9 NA subtypes. Why have we seen only a few human flu viruses in the past 100 year? What make these 3 H1N1, H2N2, and H3N2 distinctive? What implications might that have for the next pandemic?
7. how is whole genome analysis useful? Are we gaining important knowledge already? What are they?
8. Malik Peiris said pandemic is extremely likely within next 10 years. What is your view? What are the chances that this pandemic would be caused by H5N1? What about H9N2?
9. Is there any significance to the fact that some of the H5N1 has the same or similar internal genes as the H9N2 that have infected humans? What would be the implications for pandemic potential of either one?
10. If H5N1 turns pandemic, what might be the most likely mechanism based on current infor? Reassortment? Mutation? Mammalian host?
11. the latest paper in emerging infectious diseases on genomic signatures show a lot of correspondence with your work. Can you comment on the significance of that?
12. what is the significance of PB1-F2

please, ask the important questions first !


1.) what’s your estimate of the probability that there will be H5N1-pandemic in the next 5 years ? Please give a number for the probability.
2.) what’s your expectation value of the number of (human) H5N1-deaths

 in the next 5 years ?
3.) why do you think experts are so reluctant to give such numbers

and discuss them ?


[replace 5 with 4 or 3 or 6, if you prefer]
your question 8.) is too unprecise here.

Wow. What an opportunity, and thanks to both of you. Here’s my question:

According to oral histories, prior to the 1918 flu there seems to have been several waves of flu in the years preceeding that were similar but less virulent, giving people some measure of immunity to the virulent strain that swept through in 1918. My question is:

What makes a flu more — or less — virulent? What are the chances that H5N1 will become less virulent as it moves toward a pandemic strain?

Does he think that the CFR is likely to change if/when H5N1 goes pandemic? If yes, based on what?

Does he think that a “pre-pandemic” vaccine (such as are currently in development) using current strains of the virus will truly offer benefits or protections against a pandemic strain that may mutate? Will such a vaccine offer any protection, even if less than perfect, against what may turn out to be the primary pandemic strain (which we can’t develop a true vaccine for until it occurs/mutates)?

In other words, if such vaccines are offered, is it worth the risk to take it, knowing it may not fully protect (or protect at all) against future forms of the virus?

What practical advice would you give to a family looking at the potential pandemic(s) in the near future for their survival? What are you telling your own family and friends to do?

If you could advise those of us who personally know members of government, what would you have us tell them to do?

The last I heard, JKT was intending to sequence more museum bird specimens from before 1918. I would like to hear any breaking research news that he hasn’t published yet (…of course!).

NJ. Preppie – at 11:00 The last I heard, JKT was intending to sequence more museum bird specimens from before 1918.

He already did.

This one is available free. 1917 Avian Influenza Virus Sequences Suggest that the 1918 Pandemic Virus Did Not Acquire Its Hemagglutinin Directly from Birds

This one is abstract only: Relationship of pre-1918 avian influenza HA and NP sequences to subsequent avian influenza strains. Avian Dis. 2003;47(3 Suppl):921–5

Abstract: Wild waterfowl that were captured between 1915 and 1919 and preserved in 70% ethyl alcohol were tested for influenza A virus RNA. Most of the HA1 domain of the hemagglutinin (HA) gene segment was sequenced from one bird, captured in 1917, that was infected with a virus of the same HA subtype as the 1918 human pandemic virus. The 1917 HA sequence is closely related to modern avian HA sequences, suggesting little drift in avian sequences in 80 years and that the 1918 pandemic virus probably did not acquire its hemagglutinin directly from a bird. A 151-bp fragment of the nucleoprotein gene segment was sequenced from two pre-1918 birds and compared to avian and mammalian influenza strains. The 1917 avian NP sequences are also closely related to modern avian sequences and distinct from the mammalian clade in which the 1918 NP sequence is found.

anon 22. Thanks. You can tell by his previous responses that he is a ‘good man’.

If I could make a suggestion based on personal experience…one gets bored answering questions that have been asked several times over…

…it would be really neat to come up with unique questions that he could get interested in and would challenge him…that is the best of all worlds.

I’ll keep thinking and see if I can come up with one.

There was only one brant goose found to have H1N1 before 1918. That was a 2002 report. Even as of 2005 reports, I have heard of no other pre-1918 H1N1 sequences being found. The Smithsonian Brant goose sequence differed from the 1918 pandemic strain by some 25%. Contemporary North Amnerican bird H1N1 match up to the 1917 Brant goose sequence by 95–98% identity. Subsequent sequencing of H1N1 bird strains may identify astrain more similiar to the 1918 pandemic strain. The 1918 HA has 28 amino acid differences from the avian consensus sequence. The pandemic sequence is not consistent with a known avian or swine reassortment or adaptation. Until the origins are understood we may overlook where the next pandemic is coming from. (referencing from Journal of General Virology84 (2003) Reid and Taubenberger).

So I wanted up to the minute information on any new sequences from any pre-pandemic creature, avian or mammal, that might have had some version of H1N1.

Another question: As JKT’s report says there are 28 amino acid changes in the 1918 HA versus the avian consensus sequence, how many changes does H5N1 have from the avian consensus sequence?

anon_22 – at 11:10

So are you saying, that Spanish Flu did NOT jump directly from birds to human? I thought it had??

And you said little drift in Avian sequences in 80 years?

That seems like good news, in terms of H5N1

Do virulent pandemic strains of influenza have any unique characteristics that allow them to survive in the environment and spread more easily? For instance, are some more ‘sticky’ than others in that they adhere to surfaces better, survive in heat or cold better, have shells or structures that protect them from heat, drying, light? Do some penetrate more easily into hosts? Are some smaller and lighter and more likely to be aerosoled, or otherwise more easily transmitted? Are current likely pandemic strains more or less environment hardy than typical avian flu virus?

anonymous – at 12:33 anon_22 – at 11:10

“So are you saying, that Spanish Flu did NOT jump directly from birds to human? I thought it had??”

Perhaps this phylogenetic tree from the above paper might give a better idea.

Phylogenetic analysis of a portion of the influenza A virus HA gene.

Monotreme. You should be composing the question I am going so you take this one and run with it if you want.

H5N1 seems to be and has been adapting to humans. Existing thought seems to indicate that this could not happen within avian populations and would only occur if H5N1 was circulating in large numbers of mammals.

Serology studies of the H7N7 outbreak in the Netherlends indicated H7 had a high degree of transmissibility while serological studies with H5N1 in Asia seem to indicate few asymptomatic infections.

Yet, the virus’s transmissibility now appears to be more efficient H-H than B-H even though it is still overall relatively inefficient.

Are there any mammals that we should expect H5N1 won’t infect.

Is this virus circulating in an unknown mammalian that is a further vector in the link both ways between birds and humans.

With the steady state of acceleration in adaption to humans, the large raw materials (Pig populations and people in China since 2001), and the geographical explosion that occured after Q lake last years…

…I know your professional opinion has to be..we don’t know…but I am asking for your personal opinion as a scientist…

do we have weeks, months, years or decades?

Sorry, I’m not going anywhere at the moment, I just want Monotreme as well of the rest of my colleagues to improve it if it raises significant issues for everyone. Thanks.

Thanks anon_22, but much of this is over my head. Think I asked this question back at the time of the Karo Indonesia cluster, but after Dr. Taubenberger and his crew found the H1N1 virus responsible for the Pandemic in 1918 and identified it as having been of bird virus origins, was there any evidence within these samples or in his reconstruction of any segments with origins other than bird or human, i.e., perhaps swine? wild animals? Barry’s book seems to indicate that the second and most deadly wave probably originated in Kansas and then went on to spread from there. What where the prevailing animals found there then? Was it domesticated pigs? Possibly some species of wild animals? Do not have any idea what would have been most prevalent back in 1918. Suppose what I am asking is what we do not have answers to at this point in time, as there seem to be few tissue samples from back then. Sorry if I put this question akwardly, but it is very confused in my mind. This worries me more, because if this did happen here in Kansas, where even in 1918 people probably did not live cheek to jowel with their domestic animals, China, Indonesia, and other Asian countries, and as mentioned in Gojus thread, Africa, are loaded with accidents waiting to happen. Not very comforting. Thank you Dr. Taubenberger, for all of your work on this issue and for taking the time to answer questions. Miss seeing Niman’s contributions here. Thought he was back, but have not seen anything posted by him for a long time, other than on his own site. Come back Henry! I was always able to sort through your contributions to find something that contributed to my understanding, even if many of the details were over my head.

I know this thread is ‘Questions for Taubenberger’, but I’m thinking, let me see if I can tackle some of these questions, so that a) folks can get up to speed with each other’s questions, b) those who want to ask more in-depth questions can do so, and c) he can tell me how much I got right, :-).

In any case, I’m not meeting him for another 10 days, so maybe we can take this chance to discuss his work and then summarize our questions.

First of all, the origin of the 1918 pandemic virus:

why is it said to be ‘avian-like’?

If you take the HA protein of the 1918 virus, out of 41 amino acids that are known targets of immune responses, and therefore most likely to change once it starts circulating among humans, 37 of them are still avian, showing that it had not spent a long time in humans.

In addition, to evade the human immune system, the virus mutates and acquires ‘glycosylation sites’ to mask the antigenic sites. Avian viruses have 4 of these, human-adapted viruses have an additional 5. The 1918 HA had only 4.

2 Why does JKT think it was not avian?

The following figure shows how the 1957 and 1968 HA’s, acquired by reassortment, were far more typically avian than the 1918 one.

The phylogenetic tree I posted earlier (at 13:12) was from comparison of one portion of sequences from the 1917 Smithsonian specimen, which contained 24 antigenic sites. The 1917 sample matched the consensus avian sequence at all 24 sites, whereas the 1918 pandemic virus differed in 3 of them. If you look at the Gs/Alaska/917, you can see that it is most closely related to some North American avian sequences from the 1980s. This means that there was very little change in >70 years of evolution in birds. So the 1918 pandemic strain is highly unlikely to have originated in the same way as this whole clade of avian viruses.

It is also interesting to note that the 1918 HA is most closely related to the swine isolate in 1930, which I think was the earliest isolate before JKT’s work on 1918.

So in terms of relationship to the avian clades, it is the most avian-like of the mammalian viruses, but still firmly placed in the mammalian clade.

The question of pigs

Since it doesn’t seem that the virus came directly from birds, did it go through pigs as intermediate host?

Historical records show numerous accounts of outbreaks of flu in pigs at around the same time as the human pandemic. The question then becomes, did the virus pass from pigs to humans? Or from humans to pigs?

Veterinary records before 1918 appear to have no mention of any flu-like illness. So it is likely that the outbreak in pigs at least did not precede the human pandemic.

We can also get some clue from assessing the rate of evolution in swine, from studying the result of an introduction of an avian H1N1 into swine in Europe in 1979. Sequences isolated after the virus had circulated in swine for 20 years showed 17 differences in the HA with the consensus avian sequence, whereas the 1918 virus had 28 differences.

That is, after 20 years in swine, it had shown fewer changes than the 1918 virus. This, together with the absence of veterinary reports of swine flu before 1918, shows that it is unlikely that the virus had gone from avian to pigs to human.

So what JKT says is something like this, I think :-), “the 1918 virus is an avian-like virus that had adapted to humans, and had probably arisen from an ancestral source that was in evolutionary isolation (from our current known species) until shortly before the pandemic.”

Don’t know if I got that right. :-)

One more thing that might be important to point out.

Characterization of the 1918 influenza virus polymerase genes

The polymerase gene complex (PA, PB1, PB2) of the 1918 virus was largely avian-like, with a small no of differences (19 differences, 5 in PB2, 7 each in PA and PB1). Of these 19, 10 have remain unchanged since entering human hosts.

Subsequent reassortments in 1957 and 1968 pandemics had resulted in a different PB1 each time, but the PA and PB2 in the current circulating human viruses are all descendants of the 1918 H1N1. Since these changes very consistently distinguish human from avian viruses, they may play vital parts in the pathogenesis of human disease.

This had been discussed in previous threads significance of polymerase gene but I will just give one example. Of the 5 changes in the PB2 gene segment acquired in the 1918 virus, they have been consistently present in all human samples (283), but only present in 5 out of 253 avian samples. What’s more these 5 were all HP H5N1, HP H7N7, and one H9N2 strain that was able to infect humans.

This means that wherever the 1918 virus got those changes from, they are extremely important in determining the ability to infect humans.

My questions:

• Is there any biological reason to think that if H5N1 becomes a pandemic strain, it must become less lethal? If so, what would the mechanism be? I realize it might become less lethal, I’m only asking if it must.
• What is the explanation for long areas of perfect identity between flu viruses isolated in different years? AY747617.1 and DQ419819 are the accessions of two H5N1 HA gene sequences from swine isolates from 2 years apart. They are 100% identical. DQ419819 was retracted by submitters. (More info on retracted sequences here.) M73513.1 and DQ280229.1 are two PB2 sequences from swine isolates that are about 30 years apart. M73513.1 is from a H1N1 virus isolated in 1977. DQ280229.1 is from a H1N2 virus isolated in 2004. DQ280229.1 looks like a recombinant and a reassortant. The identical sequence is from nt 217–1878 of DQ280229.1. So, over 1500 nts of identity. DQ280229.1 was deposited by a group from Wisconsin. M73513.1 was deposited by Webster’s group in Tennessee.
• Do you agree that some strains of H5N1 are now better adapted to infecting humans than they were a year ago? If so, do you think it is possible that they are under selection in a mammalian reservoir? Do you think mammals as well as birds should be tested for H5N1 infection?
• Do you think we are closer to a pandemic than we were a year ago? If so, why?

Thanks for considering these questions.

Anon 22,

When will your interview with Dr Taubenberger be posted???

Dr Inglesby???

THANKS for the excellant “legwork”!!!

SCWAZ – at 21:55

I won’t be seeing either of them till after next week, after which I will try to post when I can, bearing in mind that I will be travelling so it’s kinda unpredictable. I did say definitely before the end of this month. I wasn’t going to post this thread till later, but the Nabarro discussion kinda jumped the gun for me. :-)

Why was the 1918 H1N1 so lethal since it did not lose any amino acids in its NA segment or gain any amino acids at the HA segment cleavage site? By today’s definition, it would not even be classified as High Path. Should we be concerned about a Low Path North American H5N1 that evolves toward a 1918 H1N1 even though it has no multiple basic amino acids at the HA cleavage site?

Mamabird – at 22:34 …a Low Path North American H5N1 that evolves toward a 1918 H1N1 even though it has no multiple basic amino acids at the HA cleavage site…

Sorry for the thread interuption - a quick question on critical information: Are you speculating or is there information that you’ve seen, regarding H5N1 evolving to H1N1? Would you mind sharing it?

What info have you seen that demonstrates that NorAm H5N1 “has no multiple basic amino acids at the HA cleavage site”?

Thanks

Anon_22

I read the Goju thread, and read Dr. Nabarro state that Indonesia is a “mess”. I am not in the scientific community so alot of the scientific talk goes over my head too, so I don’t have anything but an everyday regular person question to ask. What I’d like to know from an expert, any expert, is this:

1. I have read many articles about the citizens throwing chicken carcasses into rivers, in one case the dam was stopped up, last night I read where one village along the Sampean river has an outbreak after citizens in another village threw carcasses into the Sampean river. I’d like to know what an expert thinks about this going on and how it may be contributing to the situation there. This is happening all over the place there.

2. I’d like to know if an expert thinks Indonesia has really done too little, too late, do they think there is hope that the “mess” can be reversed there and if so what will it take? I’d also like the truth on that question from any expert. I am not familiar with the person you are asking the questions to so maybe this isn’t the right person to ask, but I’d like to know.

3. Just exactly what is the “mess” there? Truth please, I can handle it. Was giving out all this Tamiflu in Cikelet really a good idea?

You can change my verbage in my questions too, I am not very good at getting things phrased correctly.

This whole situation there has me very frustrated.

Thank you Anon_22 for everything you are doing.

Anon_22…Question.

Given the current situation, are you (Dr. Taubenberger) and your family planning on practicing social distancing in the event of a near time pandemic and are you currently setting aside provisions for such?

If the answers are yes and yes, a lot of my other questions will have already been answered. ;)

When you notice that the human-to-human transmissibility of H5N1 has improved and is on the verge of starting the pandemic, will you be willing to tell the MSM about it? Will you be willing to tell FluWikians (anonymously or not)?

anon_22, thank you for all your contributions to this thread, you have helped me better understand this whole situation. Your answers to my questions clarified a lot of my confusion. Let’s hope that further detective work by Taubenberger and others will find the missing link between birds and humans back then and possibly lead us to find the probable mammalian? link which is suspected now in places like Indonesia/China. On the other hand this all may be moot, or end up like the chicken or the egg argument. Plan on trying to do the last of our preps in the near future. Personal feelings are that the odds are that we are closer than ever to the tipping point. Looking forward to reading the good Doctors answers to the excellent questions posed by some of our more expert contributors.

Monotreme – at 21:52

“Is there any biological reason to think that if H5N1 becomes a pandemic strain, it must become less lethal? If so, what would the mechanism be? I realize it might become less lethal, I’m only asking if it must.”

I asked Dr Taubenberger that question in May. The short answer is no, there isn’t. But I will ask it again for more detailed elaboration.

anon_22 – at 20:40

I asked Dr Taubenberger that question in May. The short answer is no, there isn’t. But I will ask it again for more detailed elaboration.

Did you post his answer before? If so, I missed it. Very important, IMO. It blows the 2.5% rationale out of the water. I don’t know what it’s going to take to get people to face the real worst case scenario, but I’m going to keep trying.

This may not be a fair question, so don’t ask it if it appears rude, but I’d like to know if Dr. Taubenberger would be willing to publicly say that the real worst case scenario may be a CFR of 50% and that we should include this possibility in our planning. If he believes this, I assume he must have communicated this fact to the administration, yet, they are not acting as if this is in the range of possibilities.

Monotreme. I will bet you that after the pandemic…meeting notes will come out that they were having exactly the same debates behind closed doors that we have had on flu wiki…

…and that your innovative ideas have been scooped and have been the basis for at least some of those behind the door meetings.

When we nominate you for the Nobel…would you like us to do it under Monotreme…it only seems right!!…you can wear a mask to the party.

Thanks Tom DVM,

I write here hoping I’ll be scooped. A little bit different from what I do under my real name ;-)

If I and the people I care about, which includes my fellow Fluwikians, survive the pandemic, that’s all the reward I need.

/:0)

And by the way…they have the right to scoop your material and you may want them to scoop your material…

…but they have an obligation to give you the credit for the scooped material whether it is in a meeting of the WHO, CDC or the White House.

What the Chinese and some of my other friends have not realized is that…science without scientific principles and philosophies is not science…it never was…and never will be.

Monotreme - You are a humble guy, but I think a truly great one! Thank you!

Monotreme,

I did. I don’t remember when before, but the piece i wrote up on the Goju needs help thread certainly has that. But of course we can and should re-visit that question.

Question for Dr. Taubenberger:

If we understand Dr. Henry Niman’s theory correctly, it is possible, a la Recombinonimics (and here anyone feel free to jump in and correct), to accurately predict, if not the ultimate pandemic strain, then some important variants along the way.

Dr. Taubengerger, do you think Dr. Niman’s theories have validity, and if so, to what degree?

anon_22, so, now there are many questions. Which of these will you select ? How many questions may be asked in total ? Will there be some democratic selection process or will you just decide by yourself which of the questions are going to be asked ?

anonymous – at 01:59 Question for Dr. Taubenberger:

“If we understand Dr. Henry Niman’s theory correctly, it is possible, a la Recombinonimics (and here anyone feel free to jump in and correct), to accurately predict, if not the ultimate pandemic strain, then some important variants along the way. Dr. Taubengerger, do you think Dr. Niman’s theories have validity, and if so, to what degree?”

Again, JKT and I had some long discussions about this. He says recombination just doesn’t happen in flu viruses except very rarely, which means that there is no indication that anyone can make such predictions to any usable degree.

anonymous – at 02:36 “anon_22, so, now there are many questions. Which of these will you select ? How many questions may be asked in total ? Will there be some democratic selection process or will you just decide by yourself which of the questions are going to be asked ?”

Well, as I said earlier, I’m not meeting with him just yet. So we can let this thread be sort of a discussion thread as well. Some of the questions may already be answered by the time we get to the interview. As I said in my first post, I will most likely consolidate the questions and ideas to try and have a meaningful and in-depth discussion. Don’t expect me to do a laundry list, bullet point Q & A. I would much prefer trying to take our overall knowledge and ability to wrap our minds around difficult problems to a deeper level, than listing information that you can get by searching journals.

anon_22 read the thread, my questions are more than covered. I want to thank you again for all your work here and for bringing this to us, and your patience with those of us like myself with less scientific backrground than some. I will look forward to your report when you have a chance to talk to Dr. T. guess it’s morning where you are…I got to go to bed!

also ask him about the niman-Canadian swine thing. How could it be that there were zero changes on the nucleotide-level in large portions of Tennesse/77 during decades.
And why Webster,Olson etc. ignore this and leave it uncommented and why they also don’t comment on the ovious recombinations in those swine viruses.

Z – at 23:12

“What info have you seen that demonstrates that NorAm H5N1 “has no multiple basic amino acids at the HA cleavage site”?”

I don’t believe there is any speculation involved in stating that Nor Am H5N1 has no multiple basic amino acids at the HA cleavage site. As to available sequences, please note the following:

A/Mallard/Wisconsin/428/1975

A/duck/Minnesota/1525/81

A/gull/Pennsylvania/4175/83

All of these bear the signiture “RGLF” at the cleavage site.

As to the more recent findings of H5N1 in Michigan, Maryland, etc., the USDA would have to declare that these viruses were High Path if the HA had the additional amino acids, because, by definition that is High Path. The Michigan samples have been fully sequenced and USDA has declared Low Path, so, even though they have not made these sequences public, they have only the “RGLF” signiture at the cleavage site, otherwise they would be High Path.

As to the most recent samples, they are being fully tested and sequenced, but the PCR gel obviously revealed a normal length in the HA1 segment, meaning no additional amino acids, and therefore Low Path by definition.

Hope this helps.

Anon 22:

Thanks for taking on these interviews. All excellent questions. If you have a chance would you ask if dolphins and whales have been ruled out as a potential mixing vessel for flu. If not, could he provide an update on findings? Thanks.

Hi anon_22! Many thanks to you, again, for all your hard work. It’s truly appreciated.

My suggestion would be to ask JKT if there is something that FluWikians, as a group, could do for HIM (i.e., research, tracking down data, reaching out to others via our personal networks; perhaps there is a specific area of the world he is uneasy about, that we would be able to study intensively). Offer him the opportunity to assign tasks to us as though we are his personal cadre of special assistants.

It has taken me a long time to start figuring out what to write about this, this ‘conversation’ with Taubenberger. It’s a little weird, cos I had an almost 3 hour discussion with him. It was profoundly educational at the time, and now I’m left with the feeling that I know less than I thought I did.

Or to put it more precisely, it isn’t so much the content of what we talked about, but the way that he approaches problems that makes it all so profoundly powerful.

I was reading ‘The Great Influenza’ tonight, and I encountered this description of one of the most important scientists of the time, William Henry Welch at Johns Hopkins. It struck me that what John Barry was saying that Welch was NOT, describes best (although still inadequately) what I experienced when talking to JKT. I am going to quote some excerpts:

“His failing was this: in science as in the rest of his life, he lived upon the surface and did not root. His attention never settled upon one important or profound question.

“The research he did was first-rate. But it was only first-rate – thorough, rounded, and even irrefutable, but not deep enough or provocative enough or profound enough to set himself or others down new paths, to show the world in a new way, to make sense out of great mysteries.

“The greatest challenge of science, its art, lies in asking an important question and framing it in a way that allows it to be broken into manageable pieces, into experiments that can be conducted that ultimately lead to answers. To do this requires a certain kind of genius, one that probes vertically and sees horizontally.

“Horizontal vision allows someone to assimilate and weave together seemingly unconnected bits of information. It allows an investigator to see what others do not see, and to make leaps of connectivity and creativity. Probing vertically, going deeper and deeper into something, creates new information. Sometimes what one finds will shine brilliantly enough to illuminate the whole world.

….

“To see questions in these ways requires a wonder, a deep wonder focused by discipline, like a lens focusing the sun’s rays on a spot of paper until it bursts into flame. It requires a kind of conjury.

“Welch had a vital and wide curiosity, but he did not have this deep wonder. The large aroused him. But he could not see the large in the small. No question ever aroused a great passion in him, no question ever became a compulsion, no question ever forced him to pursue it until it was either exhausted or led him to new questions. Instead he examined a question, then moved on.”

I will have to think some more to put together the best of what I learnt from talking to JKT.

Thanks for the effort your giving with this, Anon-22. Be sure, I’d think,to start a New thread when you do want to post your findings. I have to admit I wasn’t positive what you meant by the above, ie if you thought Dr. T was as John Barry described Welch, or that You felt like that yourself in the conversation. Perhaps my fuzzy brain, it’s late. Don’t worry about it being too perfect when you post, we’ll hash it out as you know if we aren’t clear. Perhaps you’ll even get clearer about how you felt about it from the conversation!

…oh dear…

one other thing which I’d like to mention in this context is, that you often have disappointments with such research. Some ideas don’t work out, some work was invain. It’s important to accept this and continue nevertheless and to be able to abandon some initial ideas and to see the new paths which are opening. Some people are particularly reluctant to do this.

you can suitably summarize JKT’s thoughts by just giving his subjective estimates about pandemic probability and severety for a timeframe (other than 5 years ?) of your choice.

funny how just a few hours ago i was thinking about creating a summary.summary series of wikipages - just because i’m still trying to see the big picture and find out what’s missing - i feel it’s worthy of our efforts to create summaries of some threads

part of this is what in open space technology (ost) speech they call “butterflies” and “bees” - people who go from group to group, from conversation to conversation, cross-polinating and finding links

anon_22, i truly don’t know if you liked the conversation or not - possibly a mixed-feelings thing - we’re listening

thank you

“what John Barry was saying that Welch was NOT, describes best (although still inadequately) what I experienced when talking to JKT.”…

Sounds positive to me. Thank you and Dr.Taubenberger. Will check back for more, when you’re ready.

annon_22: Did Dr. Taubenberger happen to mention whether scientists, at NAMRU perhaps, have actually been able to study the most recent Indonesian human H5N1 samples?

I see that some of you didn’t get what I mean. I meant that Welch was not the great scientist that Taubenberger is. JKT asks the most fundamental questions that a lot of scientists have forgotten to ask, or have accepted as true without very stringent testing. In order to write up and fully explain what I learnt, I want to go back and re-read quite a lot of the studies by both him and others, just so I can verify what he is saying and also that I understand correctly what he is saying.

anonymous – at 02:43 you can suitably summarize JKT’s thoughts by just giving his subjective estimates about pandemic probability and severety for a timeframe (other than 5 years ?) of your choice.

Pixie – at 07:16 annon_22: Did Dr. Taubenberger happen to mention whether scientists, at NAMRU perhaps, have actually been able to study the most recent Indonesian human H5N1 samples?

The short answer to both questions is he doesn’t know.

he doesn’t even know his own subjective estimates ? Can’t be such a great scientist then… So, to save his reputation, let’s assume that he doesn’t want to tell them to anon_22 instead.

he doesn’t even know his own subjective estimates ? Can’t be such a great scientist then …

LOL

A bit like saying “this is a bad, bad fork because it has many pins and all are equal length - I want forks to have a pin that’s longer than the others and you have to give that pin to me - otherwise I’ll keep looking at you from above, as incompetent and/or liars”.

But I do agree with “anonymous” on one thing: it’s “estimates”, not “estimate”.

Actually, every time I look at it, it’s not like a fork at all, but more like a hydra.

Re-configuring H1N1(1918) combined great foresight with a sustained effort by a large team of researchers for more than a decade.

Their research will go down as one of the great scientific feats of all time…they deserve a Nobel and will probably get it…soon.

still thinking about the fork - it is really deep in flesh so we can’t know the length of the pins

lugon – at 09:49 “I want forks to have a pin that’s longer than the others and you have to give that pin to me…it’s not like a fork at all, but more like a hydra.”

What?? The length of pins? I don’t get it…

Getting sidetracked. Good sterling; at least it’s a sharp fork.

Swann had a great suggestion, “My suggestion would be to ask JKT if there is something that FluWikians, as a group, could do for HIM (i.e., research, tracking down data, reaching out to others via our personal networks; perhaps there is a specific area of the world he is uneasy about, that we would be able to study intensively). Offer him the opportunity to assign tasks to us as though we are his personal cadre of special assistants”

crfullmoon now that is the best question to ask. His time is focused on research and here we looking at the whole picture. Together we can see the forest for the trees, and have a better heads up to when and how it is going to happen.

OK, I just wrote up the first installment here

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