Pandemic Influenza: Science, Economics, and Foreign Policy: Session One: The Science

This session was part of a CFR symposium, Pandemic Influenza: Science, Economics, and Foreign Policy, which was cosponsored with Science Magazine.

LAURIE GARRETT: Good morning, and good morning to all of you on the Internet. My name is Laurie Garrett, and you are here in the Council on Foreign Relations in New York on a grim, wet, chilly day. Thanks to all of you who managed to forge through the nasty weather. And I expect that we'll have stragglers coming in as a result of the weather problems.

I am the senior fellow for Global Health here at the Council on Foreign Relations, and I welcome everybody who is both here and in cyberspace with us.

In a few moments my colleague, Jon Cohen, will tell those of you out in the cyber world how you can actively participate all day today via Twitter. Jon is the outstanding, infamous, notorious, famous science correspondent for Science Magazine, which is our co-sponsor today. It's a first for the Council on Foreign Relations. We embrace it wholeheartedly and hope it will be the beginning of many more to come, for this symposium entitled "Pandemic Influenza: Science, Economics, and Foreign Policy."

On August 24th, the President's Council of Advisers on Science and Technology, some of whom are with us today, so-called PCAST, issued a remarkable analysis of what's in store with the H1N1 virus, the so-called swine flu, and the likely pandemic impact this fall on the United States of America.

The PCAST offered a scenario -- not a prediction, let me say -- a scenario that suggested the virus would indeed return, having already been here in the spring, for a second wave, and that we would see it appear sometime in September and be peaking right about today in the United States, and that sometime, by the end of the year, roughly half of the American population would have had H1N1 influenza.

The PCAST warned that this H1N1, despite being a not terribly dangerous virus in and of itself on a scale of influenza dangers, would overwhelm many of our hospitals and pose a great burden to our intensive-care-unit capacities across the country.

After circulating in the southern hemisphere for the last three or four months, H1N1 did indeed return as forecast, or shall we say scenario'd, by PCAST and has now been back in most of the United States for at least two weeks. It is indeed surging very rapidly around the country.

On Tuesday, Dr. Ann Schuchat from the Centers for Disease Control opened a press briefing with these remarks: "Unfortunately, we're seeing more illnesses, more hospitalizations and more deaths from it. Flu is widespread in 37 states. That's up from 27 states just last week. Unfortunately, 19 more pediatric deaths from influenza got reported to us this past week. We're now up to 76 children having died from the 2009 H1N1 virus." She means in the United States.

To put that in context, in the past three years the total pediatric influenza deaths ranged from 46 to 88. We've had 76 children dying from the 2009 H1N1 virus, and it's only the beginning of October.

There's a great deal of uncertainty about this flu pandemic. One thing is certain: It is a worldwide event, and it is occurring in the dawn of our age of globalization.

With us today is a stellar group of scientists -- some of them PCAST members, as I said -- analysts, journalists, and, as usual at the Council on Foreign Relations, a highly diverse and intelligent audience.

Before we jump into the subject at hand, a few quick bits of housekeeping and a set-up for what we're going to experience today. We have three panels with two short breaks. And because this is live on the Web, we're going to ask that the audience that's physically here in New York please clear out quickly during breaks and come back quickly during breaks so that we stick to our time schedule absolutely.

In addition, a couple of other things. Because we are live on the Internet, absolutely no wireless devices can be on in this room. It's not just we don't want them to ring; we don't want them to interfere. So PDAs, cell phones, laptops, whatever they are, please turn them off.

We welcome that webcast audience. And as I said, Jon is going to tell you how you can twitter. And because this is the first big event co-sponsored with Science Magazine, we really want to thank and welcome all the folks from AAAS and Science for their participation and the tremendous help we got in organizing today's event.

We also want to thank Council member Richard Brown from Philadelphia, who generously provided some personal support for today's event. All of the proceedings will be available to you after today on our website, CFR.org, and on the Science website.

So, finally, I just want to hand things over to Jon Cohen for the first panel with these words. I have had a long and storied career myself in journalism. If I had one competitor who rode me harder than any other journalist in the business, gave me more trouble, scooped me more times, it was Jon Cohen.

Jon.

JON COHEN: Thank you, Laurie. That was very kind. (Laughter.) And the feeling is mutual.

I did breathe a sigh of relief when Laurie first came to the Council. And Laurie really put a lot of effort into making this happen, and I thank her and the Council, because it really takes a great deal of coordination to make something like this happen.

As a journalist, I rely on the smartest people to be my teachers, and fortunately three of them are here with me on the panel. I've learned a lot from each of them as I've tried to keep up with covering the spread of the novel H1N1.

On my far left is Dr. Arnold Monto, who is an epidemiologist from the University of Michigan and has been covering -- studying flu probably since I was born and knows a tremendous amount about the virus. Peter Palese, who's from Mount Sinai School of Medicine, is one of the foremost basic researchers of influenza and has done really fascinating work looking at how different viruses transmit and why they transmit when they do under the conditions. Lone Simonsen, who's with the George Washington University, is also an epidemiologist and has done really eye-popping historical analyses of past pandemics.

So we're going to have a conversation for about 40 minutes. Then we'll open it up to the audience. We are not here to agree with each other. This is not to develop a consensus document. If they disagree with each other, that's just fine.

If you do want to ask questions on the Web, you can tweet your questions. And the tweet hashtag or pound sign is cfrq@a.

So I think one of the questions that most people are curious about is why is this flu different, and why should anyone care about it? And so I open it up to the panel. Is this one any different? Has it been hyped?

ARNOLD MONTO: I think they're all different. That's a standard influenza statement, that if you've seen one outbreak, you've seen one outbreak, or if you've seen one pandemic, you've seen one pandemic. And this is clearly different and a little challenging in terms of how to handle it, because it is so different.

Our two past pandemics in the 20th century, '57 and '68, had characteristics which we associated with seasonal influenza, most of the mortality in people with risk conditions -- older individuals, very young. And this one is behaving a bit differently -- high attack rate, but selecting out for problems a small percentage of children and 20- to 50-year-olds.

And that really is a challenge in terms of how you handle this by vaccination, because we can't come up with our usual recommendations; older individuals should get vaccinated. In fact, we've said just the opposite.

So this has presented a challenge, and I think it's also created a challenge in terms of mortality, trying to give scenarios about mortality, because without ventilation, without ECMO and the rest in emergency rooms, we may -- we could be seeing a much higher mortality than we are.

So it's been a challenge trying to deal with this. And part of this, which I'm sure Peter can talk about, is the fact that this is not a totally new virus. And this explains some of the phenomena that we're seeing.

COHEN: Dr. Palese, you've questioned whether this is a real pandemic. How do you see it?

PETER PALESE: Okay, let me sort of say -- (inaudible) -- there is a saying the more things change, the more they stay the same. One can look at this as a very different virus. And clearly Dr. Monto pointed out what some of the differences are with this new 2009 virus.

On the other hand, I feel it is sort of like the fourth regular seasonal influenza virus. And let me explain a little bit. With regular influenza, we have three different strains. We have two what we call influenza A viruses, and they belong to the H1N1 -- and many have seen this for a long time -- H1 meaning hemagglutinin subtype 1 and neuraminidase subtype 1 -- and H3 and 2 viruses. So the regular seasonal influenza viruses belong to two subtypes, H1N1 and H3N2, and there's a third type which is an influenza B virus.

So over the last 20, 30 years, every season, every winter season, we had three influenza viruses circulating. And what happened now is we have, in essence, what I see as a fourth seasonal influenza virus which is circulating, and that is another H1N1. So I feel that also in severity it is similar to the other three seasonal strains which we have experienced, and therefore I don't think it is sort of a virus we have to be very afraid of. We don't have to panic. This is a virus which we can handle. It's, in my opinion, a fourth seasonal regular influenza virus strain.

COHEN: What do you think, Lone?

LONE SIMONSEN: Well, I take issue with that. My perspective is in studies of the past four historical pandemics, and I also disagree with Arnold.

I think that actually these pandemics -- there are things that you can call signature features of pandemic influenza that we should pay a lot of attention to. The first one is that the burden, in terms of mortality, shifts towards younger people, especially in this one. You see actually very few deaths and severe outcomes in people over 65 years of age. That's highly unusual for influenza.

The reason why people maybe think this is mild is that actually, when you count deaths only -- and this is very unique, frankly, that we don't count more fancy, complex metrics for a burden of disease. If you started counting the years of lives lost, if you would start counting 50 years' life lost for everybody who's 30 years old who dies of primary viral pneumonia and start adding up -- (inaudible) -- so that way there's something to be said for really looking at this with years of life lost, metrics and other ways to really highlight that the burden is completely different, like a different picture it has.

The other thing that we know from pandemic, as far as pandemic flu, is that it's not over just because we're here right in the middle of the wave. It's not over yet. It's really just the beginning of our experience with this virus. We've seen it in all the past pandemics. We see over the first five years, that's when the deaths play out.

So, for example, if you look at the 1889 pandemic, most deaths happened in the third wave. If you look at the 1918 pandemic, most deaths happened in the second wave. And then in '57 and '68, it was in the first wave; so just to say that it's not for sure that everything has come yet.

So I would just say that there's definitely a different picture of it. And the signature feature, the age shift towards the young, is something that sets it apart from seasonal influenza.

COHEN: I think there's a lot of curiosity about why young people in particular and pregnant women are seeing a lot more severe disease. Flu typically causes the most mortality in the elderly. That's not happening with this. Do you have any ideas as to why the younger population is being hit so hard, and pregnant women? Is it biological? Is there an epidemiologic explanation?

MONTO: Well, I'll try to add a few things from the historic record, which I'm sure Lone can further add to, and that is, in 1918 -- and this is a whole lot different from 1918; I think Lone and I can have a conversation about that -- but in 1918 it was very clear that pregnant women were at particular risk. There are some contemporaneous curves looking at puerperal mortality, deaths in pregnant women. And there is a big spike in 1918 when this was going down on a year-to-year basis.

Women were heavily infected and quite ill, and they often lost their babies if they were in late stages of pregnancy. So this is not particularly unique. It's a little more questionable in some of the later pandemics. And because of this, we in the U.S. -- and we're one of the few countries that has this recommendation -- recommends the use of seasonal vaccine in pregnant women, because we know that this is a particularly vulnerable population.

Why in this pandemic is it so much more extreme in terms of what's going on? It's hard to say. We can speculate about that. We can speculate about obesity as an -- whether it's an independent risk factor. But I think a lot of what is going on is really based on the fact that there has been past experience with this virus. And we see this in terms of the way the vaccine is working; the fact that we only need, for most of the population, one inoculation with this vaccine, which means there is some degree of relative immunity in the population.

And there's been a debate about whether, to have a pandemic, a real pandemic, you need to have a totally novel virus. And one of the reasons we've seen partial sparing in older individuals in past pandemics is these were not totally novel viruses. There was some degree of antibody in the population.

COHEN: A challenge, Peter.

PALESE: I think I just want to sort of explain why the older population is more immune against this new novel 2009 virus. And it has to do that both the regular H1N1 virus as well as this new 2009 virus are both descendants from the 1918 virus. So the 1918 virus went into humans, and in essence we had this virus descendants of the 1918 virus until 2009. But it also went into the pig population. And the 2009 swine virus is actually a descendant and has changed less in the pig population as compared to the human virus in the human population.

And so people who have been around in 1930, 1940, 1950 actually were infected with a descendant of the 1918 virus, which is closer to the 2009 virus. So people who have been around 50 years and longer have been exposed to such a virus or a much more similar virus in the 2009, and therefore the older population is more protected against this new 2009 virus. And also the older ones have experienced many more infections with H1N1 viruses. And that explains why the older ones are better off. It's one of the few things in life -- (laughter) -- where age -- (inaudible).

COHEN: What about the kids and the pregnant women?

I mean, why are they -- is it simply that they don't have -- I mean, the pregnant woman may well have some immune memory to lots of different strains. What is it? Is it the diaphragm has a harder time clearing the lungs? I mean, any thoughts about why?

MONTO: Well, that's one of my speculations but I think it's pure speculation. You can come up with any number of theories to day why pregnant women are different from them because there's relative immune suppression as well because of the fetus, and there are many, many reasons.

I think one of the things we need to learn -- and a number of us are talking about research agendas, trying to figure out where to go in the future based on what's happening now. One of the speculations would be that there is some degree of immune suppression in pregnant women, but seeing the cases that we're seeing, seeing the virus pick out in the 20- to 50-year-olds, individuals -- you know, when the infection rates are relatively high and a small percentage of people are winding up very -- in the ICU and getting very sick very rapidly, there's something different about these people.

And we don't really understand it yet, and this should be an agenda for trying to figure out what is going on that makes people not more susceptible to infection but more susceptible to a severe outcome.

COHEN: What do you think?

SIMONSEN: Well, I think that the pregnant lady is susceptible doesn't surprise me that much. When you read in the literature you will see horrible accounts of case reports of pregnant women with systemic infections in '58 and the '68 pandemic -- the '57, '68 pandemic. So what's more intriguing to me is the two patterns that we're seeing with this one, which is the -- (inaudible) -- and it's this increased extreme risk in younger adults 20 to 50 years of age or a little older, or to 65.

And, in fact, we know a lot about it now that we didn't know at the PCAST meeting. We know that the 20-to-64-year-olds had 54 higher risk -- 54 more people end up in the ICUs and clog the ICUs. What is that?

So, in a way, we started speculating about this in our 1918 stories because it was the same situation exactly and the elderly experienced nothing in 1918. They actually had a three-fold worse time two years before in an epidemic season.

So we came up with two explanations which might actually have to be -- go together. One is the recycling that we were hearing about, that there is some immune experience in the elderly that protects them, but at the same time you have to explain why other -- young have increased risk. That doesn't explain -- the first doesn't explain the second observation.

So what is that, and is it some kind of adverse immune potentiation process, some kind of -- where the immune system is actually reacting in a way with a virus that causes the severe outcomes? So there these things.

And then you can add a third thing, which is could it be that there is a need for a bacterial co-pathogen, in come cases at least, and is it something that actually sometimes is there and sometimes is not there? And we use that to explain why the first wave of the -- in the 1918 pandemic was very mild, for reasons we don't understand clearly. It had the same footprints in every other way but didn't kill people the same way, and when it came back in the fall it did. Could it be that there was a bacterial co-infection for -- that suddenly was available?

So I think there is just so much we don't know about this and it's fascinating.

COHEN: So the bottom line is we don't know.

SIMONSEN: Yes. (Laughs.)

COHEN: If you look at the virulence here, there was a great deal of hand-wringing at the World Health Organization about whether to declare this a pandemic, and it came down to the fact that pandemic doesn't really reflect severity. And so this wasn't as severe as the H5N1 bird flu, which maybe killed 50 to 60 percent of the people it infects.

And so now the question has become, why bother getting vaccinated? And you even hear a lot of public figures standing up saying that they're not going to do it. I will state my bias. I have two younger boys who both have been vaccinated against H1N1 and I'm very happy about that. But I'm curious what you think. Would you get vaccinated, and do you think your family, your colleagues should get vaccinated?

PALESE: Maybe let me start this one out. So even though I mentioned that this 2009 novel influenza virus is really like a regular seasonal influenza virus in many of its characteristics, that doesn't mean that I underestimate influenza. Regular seasonal influenza is a very bad disease. And we all know that in the U.S. alone we have about 30,000 deaths and we have about 200,000 hospitalizations every year.

So regular flu is a very serious disease and therefore we should really use all the tools we have to combat and to fight the regular flu, and that includes vaccination. And by the same token I think it is really compelling that we should use the vaccines which are being produced and being distributed right now against the 2009 virus. So, by not taking the vaccine, by underestimating this disease, I think we are not helping us.

COHEN: Any dissent?

SIMONSEN: No. I mean, it's very clear that vaccination is the best defense we have against pandemic influenza. In fact, when you have a pandemic unfolding and really high transmission rates, it becomes very hard to mitigate with any other strategy than that.

So, from a personal point of view, I have the advantage of natural immunity at this point, I'm pretty sure.

COHEN: You're from 1918?

(Laughter.)

SIMONSEN: No, not that, but because in the May and June --

COHEN: You got --

SIMONSEN: -- our whole family experienced it. But I would still get the vaccine because what's not to love? You get a vaccine that's not risky and you have the protection, so --

COHEN: Dr. Monto, you showed many years ago the importance of vaccinating children in flu season, and indeed children have the worst vaccination rate of any age bracket in this country, and yet there is a big push right now to protect our children. They're first in line. How do you see it?

MONTO: Well, I'm not sure that children have the worst vaccination rate in this country. Health-care workers are pretty low as well. (Laughter.) I think we're doing a lot better there because there are more and more society recommendations and approach to getting -- to mandating that health-care workers, if they're taking care of sick individuals, be vaccinated.

But I think we've got two reasons to be vaccinating children here. We know that they have the highest attack rates. We also know that children, not only those with underlying risk conditions such as asthma, are being hospitalized at a very high rate -- and we're heard the quote from Anne Chuhud (ph) about the pediatric mortality that's showing up.

So there are a lot of reasons other than the fact that by vaccinating children you're actually preventing transmission or reducing transmission, I should say, to the entire community to have -- to vaccinate children with the current vaccine.

I think there's a bit of a challenge in terms of this cutoff at age nine or 10 in terms of requiring two doses. I would be happy to see children receive one dose of this vaccine because -- and this is sort of deviating from current recommendations because that's in fact what's going to happen as vaccine arrives relatively late in much of the country so that they'll get at least partial immunity and partial immunity is probably going to have not only an individual but a societal benefit.

To back up to the issue of declaring pandemics, because having been on the WHO Emergency Committee, I had to deal with -- over the telephone with some of these issues on telephone calls that went on for three to four hours. And basically the problem was that WHO, unlike the United States, had not got to the point of defining severity.

The U.S. came up with categories one though five, and we've learned that if you base this on case fatality, you can't very well figure out where you are in terms of the categories. So we had it set up but we've never really been able to implement the categorization the way we thought we would.

But WHO had never done that and there was concern that because there was so much focus on H5N1 in much of the world, especially in Asia where they had been seeing avian influenza, that declaring a pandemic would shut borders because of all sorts of things, and they needed a little time to figure this one out.

And that's why there was a delay between going from phase five to phase six. Interestingly, it took two days for each of the other increments but it took six weeks --

COHEN: There was a lot of hammering.

MONTO: Yes, exactly.

COHEN: Yes?

PALESE: So the issue is what is a pandemic? In the past, a pandemic was defined as a global epidemic -- meaning an epidemic worldwide -- plus -- (inaudible) -- its severity and a change of the subtype. So, in other words, if something was an H1 or an H3, we would not have called that a new pandemic.

So what happened with WHO now is that they've redefined or made a new definition of what a pandemic is, namely limiting it to the global epidemic too rather than severity and change of subtype.

So in a way we have now a new terminology for pandemics, namely just calling it something which goes around the world is a global epidemic, but not including severity and the change of subtypes.

COHEN: Go ahead.

SIMONSEN: Well, I just want to return to your premise for this question, which is why worry? Is it so severe, or something? And I just want to point out that I find it interesting that -- and I think it was a conclusion from the PCAST meeting that the surveillance systems we have in the United States would not be very good at tracking hostile stations and severe outcomes in young populations.

They tend to be biased towards tracking things that happen in old people -- for example the 122-city surveillance system where you are tracking the percent of pneumonia deaths per all deaths every week. And if you have -- because you have a lot of old people dying all the time, that might keep looking unimpressive because you're just drowning a real signal in a very big background.

COHEN: So you think we may be underestimating?

SIMONSEN: Well, we're just not seeing -- we don't have a good sort of picture of this specific phenomenon that you have maybe clogging up the ICUs, but you have really a drain on the hospital system. None of the systems are capturing that right now and CDC is building that right now.

COHEN: So I think a lot of journalists like this question, and I think we like it because the public is curious about it. And I don't want to over-blow it, but the doomsday scenario of this virus combining with another virus -- influenza has a weird property where it can pull genes from other influenza viruses -- and creating a really nasty strain.

What do you think the likelihood is of this mixing? The worst doomsday would be the H5N1 mixing with this one, but it could be this one mixing with any other avian influenza that we have no immunity against. What do you think the likelihood is of this mutating or reassorting, picking up other genes from nastier -- creating a nastier bug?

I know you've thought about this but what do you think, Dr. Palese?

PALESE: Influenza viruses have a very interesting genome, a very interesting genetic composition. And it has eight sort of mini- chromosomes. So we have one virus with eight mini-chromosomes and another virus with eight mini-chromosomes, and they co-infect the same host, and then you can get mixing and get a new virus out which has, let's say, four mini-chromosomes from one virus and four from the other parent. And that gives a lot of combinations.

So clearly we have the H5N1 virus, we have current 2009 viruses, and all of these mixing events can happen, and out of that a new, more virulent, more pathogenic virus can emerge. Never say never. On the other hand, I think these events are probably occurring as we speak all over the world and only very rarely a sort of new virus emerges.

So I think, yes, we cannot exclude the possibility that by this, what we call reassortment, mixing of the genes, a new virus emerges, but I think it happens all the time and very rarely a new very virulent virus emerges.

COHEN: You're not losing sleep over this possibility?

PALESE: I think it is not -- I think it's like -- I'm not waiting for a lottery win. I think it's very rare and I think it is also very rare that a new 1918-like virus would emerge.

MONTO: I agree that we've got a lot to concern ourselves with, and to lose sleep and to divert attention from the really important questions to speculation which could be endless about reassortment events producing a doomsday scenario really divert us from what we should be worrying about.

The one reassortment scenario that I worry about -- again, I'm not losing sleep over it but something that is realistic -- concerns the fact that our seasonal or formerly seasonal H1N1 viruses have become resistant to the antiviral that we most commonly use, oseltamivir or Tamiflu, and we've now got a pandemic H1N1 virus and in some regions they have been co-circulating, and you can come up with a scenario that the NAE (ph) segment, the neuraminidase segment, could reassort from one to another and give us a resistant-to-Tamiflu pandemic virus.

Again, I'm becoming more and more of a fatalist about resistance developing to the pandemic virus against Tamiflu because when this happened with the seasonal viruses, it happened in a country which wasn't using hardly any antiviral. It may have come there from someplace else.

But if it's going to happen, it may just happen, and we have to deal with various scenarios and approaches to deal with it. And I think we are doing that now. A lot of countries are not in as good shape as we are because we do have Relenza, or zanamivir, in our stockpiles. Some countries are 100 percent Tamiflu because -- and the resistant virus is susceptible to zanamivir, or Relenza.

COHEN: And just as a point of clarification for people, when people develop symptoms of flu, there are estimates that about 2 to 5 percent of people actually have two flu viruses at that time. I think that's an important point, that they can't actually mix inside of a human. And the pig can actually mix human and bird viruses as the same time.

So if we're putting H1N1, the new H1N1, back into pigs and turkeys, which has happened now, they could reassort with other avian or human viruses to create -- or pig viruses to create a new monster virus. I think that's the worry that some people have.

Lone, do you have any --

SIMONSEN: I don't know that I would lose sleep over it, but I do say I can't help having an eye towards the 1918 data, where we just had a possibility to look at this really carefully in the beautiful surveillance system in Denmark where you could see everything. In the small population you could see exactly what happened.

And you saw that in 1918 there was a lot of mobility. Everybody saw it. A few people died. And then something came back -- and the people who died were 20 to 40 years of age, just like in the major wave. And then they came back six-fold -- were six-fold higher case fatality rate in the fall.

And I'm not saying it would happen again, but I think it's prudent for CDC and others to keep in mind that they assist our president for things getting worse, and we shouldn't take our mind off of that just because it looks mild right now.

COHEN: Well, that leads nicely into the last question I'm going to ask and then we'll open it up.

The PCAST scenario had a worst-case scenario of about half the American population becoming infected. The virus would be peaking right now in this wave so that vaccination may well arrive too late to do any good. The ICUs would be overburdened, especially with the need for pediatric respirators and deaths could reach as high as 90,000.

What are your scenarios at this point? How do you see this unfolding? What do you see today? When you look into your crystal balls, what are you seeing?

MONTO: It didn't take a whole lot of prescience to be able to figure out that it was coming back this fall. And I'm still amazed when people don't realize that if you're seeing a low level of transmission over the summer besides historic precedence -- when you're seeing low-level transmission over the summer, which we never see -- summer camp outbreaks and things like that -- that as soon as school is open, things are going to start taking off. So that wasn't very hard.

Coming up with scenarios in terms of mortality, that's been very difficult because of the characteristics of severe disease. And, again, you can speculate what it would be like -- and I think this has happened in some developing countries. If we didn't have the number of ICU beds that we do have, and there has been strain on them because these outbreaks have been very focal, and in areas where there have been a lot of cases, severe cases wind up in the ICU very rapidly, especially in the 20- to 50-year-old age group.

I think the thing which people don't recognize that has happened is that there was a very strong push to get vaccine out early. And this was based on the prediction -- which, again, was not very hard to come up with -- that we were going to see disease peaking around this time and therefore if the vaccine is going to have any effect, it better be out there.

Because there was a tension between let's treat this differently from a strain replacement scenario, which is what's being used, which requires relatively truncated testing, and doing all sorts of tests in all age groups, which would have meant that the vaccine would have arrived in December-January.

And this is one of the things that the PCAST really emphasized and pushed, and other groups as well. It wasn't simply the PCAST working group. And I think that's one of the real accomplishments, that those of us who see this from a epidemiologic standpoint accomplished in the past couple of months.

COHEN: What do you think, Peter?

PALESE: I think the government should be really commended for having bought the vaccine doses and has been able to really make it happen that they get distributed very early in the season, and I think it's a real great success. And I agree with Dr. Monto that this is really -- the PCAST report was just part of that effort to really make it happen.

COHEN: Do you think it's peaking right now and that maybe the vaccine will arrive too late? In '57 that seems to be precisely what happened.

PALESE: I think if it is really peaking and that was it, I think we should be all happy, yeah.

(Laughter.)

MONTO: But in '57 there was a winter wake --

COHEN: That followed the fall --

MONTO: That followed.

COHEN: Right.

MONTO: And we know -- you know, we estimate the percent that had been infected. We really don't know. One of the things we're proposing to do with the (zero ?) survey, trying to figure up how many people actually have been infected because there's a lot of milder disease and apparent infection. So we really don't know.

COHEN: Well, that's why we have modelers.

MONTO: Yes, well -- (laughs) --

SIMONSEN: Even without models --

MONTO: -- which give us different answers.

SIMONSEN: Even without models we can just look at what actually happened in the past pandemics. And I'll just reiterate what I said before, that because the impact that's going to happen in some severe outcomes is going to play out over years, then it's not too late to get the vaccine, even if this is a peak --

And you're asking if it's a peak year. We can see some cities have actually peaked. They are coming down. If you look at the national surveillance system for CDC for this week you can see it's still going up but that's delayed by one week, so maybe we are approaching the peak.

Your last thing about 90,000 deaths, is that a good estimate of something, well, it sounds pretty reasonable to me, but then I just want to say that we really have to stress this business that it's not 90,000 deaths as usual; this is 90,000 young deaths. If that's 30 years of life lost for each one of them, it could be 300,000 years of life lost compared to a normal season where you have 30,000. So that would be a tenfold higher. So you've just got to think about it in that way.

COHEN: Okay, well, let's open it up now to the audience and to the pleaders. And do we have microphones in the room that can -- and please keep your questions as succinct, if you would. And the Tweet, again, if you would like to Tweet, it's pound or hash symbol, CFRQ&A.

Yes, in the far back?

QUESTIONER: Thank you for the panel. Michael Dal Bello from the Blackstone Group. It seems like the clear consensus is that we should all be getting vaccinations. How do you evaluate the United States' infrastructure to distribute those vaccinations? And in particular, could you compare that to best in class in comparison to other countries? Thank you.

MONTO: Well, this is sort of out of my area. We're very good at making recommendations but the question of implementation is very important one and I think it's going to vary across the country.

This vaccine has been purchased by the government. It's going to be delivered in ways that we are not used to giving influenza vaccine recently. The public health sector has been more involved in giving vaccine than in the past.

I think it, as everything, is going to vary by state and local jurisdiction. Our own county, having the University of Michigan Hospital and St. Joe's Hospital and a very academic and interested group of physicians working together, is going to do pretty well.

I'm worried about the fact that we're in the middle of, number one, a recession, which has affected a lot of the states. And our state, basically, if it doesn't have federal support, it's not being done by the state health department anymore because there's no state funds that are coming into this.

So I think this fits into the decay of public health at the local level in the U.S., which got a bit of a burst during the biodefense kind of era but which has really languished in the last few years. So it's part of a bigger picture.

COHEN: And if you haven't read the book, Laurie Garrett wrote a book about that.

Yes?

QUESTIONER: Betty Masham (ph). Last year, at a discussion here about the flu, we were told that if you get influenza, don't go to the hospital because you'll infect other people. Have enough liquids and food to stay home, and that the Tamiflu and other things would only be given to health-care workers, fire fighters, policemen. So is that the same advice this year? If you get it, stay home and hope you survive?

MONTO: Well, yeah. (Laughter.) It all depends -- it depends who you are and where you are. Certainly that is the advice that has been followed in many areas. If you are a student at the University of Michigan, you are being advised not to overburden the health service by coming in, but there is support at the student housing and the rest to take care of you in case you do really need medical care.

A very different approach has been taken in the U.K. where, at least when they were having -- I don't know what's happening now in the autumn, but at least in the spring they activated their more or less 800 number to call in. And what happened, they had a very large stockpile of Tamiflu. If you became sick and you met a case definition, you had a health-care buddy who would come and get the drug and bring it to you.

The decided that it would not be over-using the drug, because they had plenty, to do it this way. And they also used drug for prophylaxis. And this is one of the reasons I'm a fatalist about development of transmissible-resistant virus because they really didn't see resistant virus developing with very extensive use of Tamiflu.

A very complicated answer but I think the health-care system is going to differ in different places and the responses are going to be --

(Cross talk.)

COHEN: Go ahead.

PALESE: One approach to your question really is get vaccinated -- I mean, get the vaccine. I think that's sort of, I think, the safest advice one can -- and I think the best piece of advice.

SIMONSEN: I just want to offer the other point of view. When you are a patient and you think you might have this influenza and you go in, you're actually putting yourself at risk of getting it from somebody else who is sitting there having it. So that's something to consider.

The reason why CDC has recommended to not treat those who have milder illness is, first of all, to spare the supply for the more severe cases, but also with an eye towards resistance development, that it's probably a good way to delay the time until we have serious problems with Tamiflu resistance.

COHEN: Please identify yourself too, if you would.

QUESTIONER: James Tunkey. I'll introduce myself as a supporter of Laurie Garrett, and thank you for putting this all together.

My question is really about the science of the development of vaccines. With the rapidity with which this set of vaccines has been introduced, what do you think is working? And what's your sense of the different approaches to the development of multi-drug-resistant vaccines, and what do you see as the future for vaccine development? What's really working, in your view?

COHEN: Dr. Palese, you've been involved with making vaccine.

PALESE: The vaccine against the 2009 is very, very good because it's very close to the actual strain which is circulating. With influenza one always has the problem that the vaccine may not be against that particular strain which is circulating but something which was circulating last year or two years ago.

So that's not the case with the 2009. So we are very good in terms of really reflecting what is going outside in the population, what is circulating. So that's very, very good, and as -- I mean, the vaccines are as good as we can only hope for.

The second question is can we sort of -- in the future will there be a universal vaccine against all the strains, and can we make vaccines which will last longer than just one year or two years? And that is obviously in the mind of many of us in the academic laboratories as well as in industry, to really make even better vaccines.

I'm saying even better because the present vaccines are very good, but there is clearly room for improvement, making universal vaccines which are effective against all different strains.

COHEN: Yes?

QUESTIONER: Seth Berkley. If I can make a comment on the vaccines and then ask a question.

The problem with vaccines is most of them are made on eggs and this is a technology that's existed for more than fifty years. It's slow. Obviously if Avian Influenza was to kill flocks and they're protected from that, but it's dangerous, and you have to have that virus that they grow on eggs. So sometimes you can't match the virus as well as you'd like because those aren't the ones that are growing on eggs.

So technology can solve that. There hasn't been a lot of investment in new technology until recently, and I think that's changing, and I think we'll see universal flu vaccines. We'll see lots of new technologies coming out in the near future and I think that's exciting. Unfortunately it isn't here for today's new outbreak.

The question. You didn't talk about -- a lot of things come out. A lot of scandals come out. A lot of discussions about it in the media. One of the things that came out recently was a discussion in Canada suggesting that perhaps people who receives regular flu vaccine had a higher risk for severity of disease. I think that has been done away with but I think we ought to comment on that --

COHEN: And that's an interesting question, and the exact opposite finding came out of Mexico, and Seth Berkley, by the way, is head of the International AIDS Vaccine Initiative, so he knows what he's speaking about when he's speaking about AIDS -- about vaccines. Anyone want to comment on --

PALESE: Yeah, I -- I --

SIMONSEN: Well, how do they refute the --

PALESE: The Canadian problem.

COHEN: Helen Graham (ph) will --

SIMONSEN: I --

COHEN: -- be on a later panel --

SIMONSEN: I think that this was an example of a really, really difficult -- and you had a hypothesis, you really want to go see the study. You're working on it in real time. The Canadians did an amazing job working this problem up. Some of the -- the whole underlying problem with figuring this out is that there is a beautiful potential for confounding and bias in that people who are very severely damaged by asthma -- they are having problems with asthma. They are more likely to get vaccinated. They're also more likely to end up in the hospital. It's very hard to control for their -- (inaudible) -- studies. However, one of the studies I couldn't do away with, and that was a major first one they saw. I just couldn't see how you could explain that observation away. So I don't know. I think that that will give it the benefit of a doubt so that there was something.

MONTO: I'll go further than that because I -- we're one of the sites participating in the CDC observational study that has almost exactly the same design, and we just don't see it. And there are studies in the UK, studies in Australia. WHO has spent hours on conference calls discussing all this because it has enormous implications for policy and this is for unknown reasons and clearly bias confounding seems to be a problem in Canada. And I'm looking at Helen over there.

We don't understand it because in Canada, this is not simply one study. This is three or four studies coming to the same conclusion. So it may simply be the way -- remember we're working here with medically -- basically with a variety of medically attended illnesses, so it may be something -- and it's not a randomized trial. And there's something funny going on.

The other thing is we have no biologic basis for this actually being the case because if this is a problem, natural infection with seasonal H1N1 should also be a problem, and we don't have evidence.

COHEN: So you don't see it but you take the study seriously?

MONTO: Oh, we have to take these studies seriously. They're well done.

COHEN: Yes.

You've been waiting a long time. Go ahead.

QUESTIONER: Thank you. Cynthia Roberts.

You have speculated about the virulence of when the flu pandemics are more virulent than others either because of the mixing or because of perhaps bacteriological covariance, but I'm interested in the other side of the question, the pathogenicity.

Do you we know why -- in the scientific community -- why some of these pandemics are more pathogenic than others, that is they spread more? This one seems to be spreading much faster than '57 or '68. Unlike 1918. Or is that we just don't have enough data yet, we don't know, or that's just incorrect?

SIMONSEN: So I'll say something about the -- (inaudible) -- then you can say something about the virus maybe.

Actually it doesn't spread faster than the other pandemics. That can be -- the estimate that we measure which is called on off (ph) because of this frequency of this on off (ph) thing happening, and that is quite low. It's not that much higher than seasonal flu. Compared to 1918, for example, it was probably over two. Here it was just 1.4. So can't really say that it is transferring faster or transmitting faster.

COHEN: Explain what the two and 1.4 mean.

SIMONSEN: Okay. So it simply means that for every person who is sick on the average today and sick, 1.4 people and when you see that traveled over many generations of infections, it leads to a very different path of an on off spread. So that's sort of the key parameter that we are trying to measure. So from all the studies I have seen they may show -- in Mexico and other -- somewhere between 1.2 infection for each person up to 1.5. So it doesn't seem that high to me, but then again you have this mystery of New York City suddenly had a huge wave in May and June and not in other cities and I think that remains completely unexplained by --

MONTO: Well --

SIMONSEN: -- mathematical models.

MONTO: Well, that's not quite true because in Ann Arbor, Michigan, and the entire Michigan area, we had -- we filled up our intensive care unit and this has been reported in the MMWR. We had a major outbreak, and I think the thing that is different, we speculated on --

COHEN: You mean last Spring?

MONTO: Last Spring. Last Spring. And we're not seeing a whole -- we're seeing university outbreaks. We're not seeing a whole lot in the community because I think we had a lot of our infections last Spring, and what we all speculated about was what the effect of high level air travel would be on the spread, and I'm talking about dissemination rather than the person to person spread. Dissemination of the infection, and we -- now we know because it showed up in so many parts of the North America at the same time and people were coming back from Spring Break and all the rest in Mexico and it clearly was impacted by what we think was a high level of transmission in Mexico, which had to be the case, since it came from all over, and air travel into various parts of North America.

COHEN: But Dr. Palese actually studies what makes influenza viruses nastier, if I can say it that way. Also I should have mentioned. Their bios are all on the web and in your packets which you get.

Dr. Palese, what do you think?

PALESE: Yeah, we know really a lot about -- (inaudible) -- influenza viruses. We can study for example, the 1918 virus in the laboratory under high containment, the conditions. So we really understand a lot about the molecular signatures of these viruses and really I think that this helps us to sort of gauge how virulent a particular virus is and what potential it has. So we really know, for example, that this -- now the 2009 virus lacks certain signatures which other pandemic influenza viruses have and that also I think goes a long the way to suggest that this virus is not an 1918 like virus.

COHEN: Or '57 or '68.

PALESE: Well, I would add also, it won't be like 1957 or 1968 virus.

COHEN: All right.

Go ahead -- (inaudible) -- and if we have any Tweaters (sic) tweating.

QUESTIONER: Tom Wilson (ph), Cornell Medical School.

Sir, I think we're all aware that the anti-vaccine movement is having a field day on the Internet and on media outlooks like Fox News and so on, causing productions in vaccine uptake, and it appears to be a pretty unholy alliance of the ultra right and the ultra left working together to sort of hit with strong anti-tactics, and I'm not sure we're countering these people very well, and one of the things I do in my spare time is counter the AIDS denial as to people believe HIV is harmless or doesn't exist, and who led to the deaths of over 350,000 people in South Africa over the past decade.

And you have to take these people on in a different style than scientists are used to. We have to develop better sound bites. We have to develop better discussion. You don't really -- you can't really debate these people, but you have to develop the counter methods. For example, you hear that we shouldn't take flu vaccines because the mercury will kill us.

Well, Paul Offert (ph) in the New York Times last week pointed out that there is less mercury in a flu shot than there is in a tuna fish sandwich, and that's a powerful sound bite to use against the crazy people who think that vaccines will kill you. That's just one example. We need to develop anti-tactics to get across the message that vaccines are safe and beneficial to society, and we need to learn to deal with the crazy people who would try and stop us doing that.

COHEN: Do you have a question or --

QUESTIONER: That's really the question. How best we can develop methods to stop the anti-vaccine movement causing so much damage --

COHEN: And --

QUESTIONER: (Inaudible.)

COHEN: For me?

QUESTIONER: Yeah.

COHEN: Well, I mean, as far as a journalist's perspective on it, I think our job is to put facts forward and to also expose people and institutions that promulgate things that aren't true, and that's all we can do. There always will be people who think things that are not accurate.

I've never figured out a way to stop them. All I try to do is combat nonsense with truth as much as I can, and that's kind of it. And I will assume that in a place where we allow freedoms of speech there will always be people saying things that I think are pure lunacy. And they'll always be there.

SIMONSEN: I'd like to completely agree with you. I think there's a lot of room for improvement, virtually reaching better across the public health expertise to attract the people who are interested in receiving the facts and actually to prevent the mistrust. Actually, there are many people who sort of (inaudible) that mistrust and I think there's really a very good case for doing more in the area of psychology and communications strategy to actually relate data and so that people can really understand. I mean, we're on the same plane here. This is a disease that's threatening humanity and here is the best vaccine and you need it.

COHEN: Lori had a question.

MONTO: I also have ruined many dinner parties, Jon, over this issue, so I side with you.

GARRETT: I'm Lori Garrett from the Council. Two very, very quick ones. One, Dr. Palese, you said this particular virus, fortunately, does not have the genetic signatures that we look for that tip us off that we're looking at a dangerous, virulent influenza, but there was a report, a reliable one out of the Netherlands, regarding two individuals who appeared to have this what's called the PB2 mutation in their H1N1 so that somehow this had naturally arisen in the Netherlands.

If it could happen in two cases, why couldn't it happen in more? If you could answer that and then to the group generally, one big lesson we're getting from the Southern Hemisphere experience is that there have been very marked differences in mortality between the poorer countries in the Southern Hemisphere and the wealthier, and if we follow the Australia/New Zealand information, a lot of it has to do with really heroic intensive care measures, including artificial lungs that are essentially washing all the blood of the patients and, nevertheless, the mean age of the death group was 34 years of age.

So I guess that leads me to the question -- what does this really tell us about the difference in mortality between wealthy world experience and poor world experience or between areas with less access to health care, even rural America, versus a place like New York City.

COHEN: Dr. Palese, you want to start with the PB1F2 question and briefly explain what that is?

PALESE: Yes. So, clearly when I say this 2009 virus is like another seasonal virus, I don't mean this is a harmless virus which we should ignore. No. The regular flu is bad enough and this 2009 virus is also bad enough. Having said that, it lacks certain signatures, certain molecular signs which are associated with the 1918 pandemic and then explained in 1957 and in 1968, and that is one of the genes.

It's a short one. It has a technical name, PB1F2 and that is missing in the 2009 virus. And it could acquire this by exchanging that mini-chromosome and getting one which carries that PB1F2 or by point mutation. However -- and that would make it more virulent. However, it is sort of like if I put a more powerful engine into a VW, if I put a Lamborghini engine into a VW or a little Fiat or some car, it may not be better. It may not fit. It may not mesh and that, I think, may also be happening with the 2009.

By accumulating and getting mutations or getting this other gene, more virulent gene, it may not end up as something which is really a sports car which runs 200 miles an hour, so there is a lot which has to sort of fit and mesh in order to make a virus really a 1918 or 1957 ---

COHEN: So it's really a multi-genic process? It's more than just one?

PALESE: Yes, and, again, I mean, if you have a marathon runner, just giving him long legs doesn't mean that the guy will win. I mean, he needs also good lungs and so - and one long leg won't help either, so in a way -- (laughter) -- by giving one new virulent stream into that doesn't make it really, in all cases, more virulent.

COHEN: What about the Southern Hemisphere versus the Northern Hemisphere and what Lori was pointing out is, I think, really astonishing, what's happened in Australia, New Zealand and the lengths they've gone to, to rescue people who otherwise would have died, and they've said as much, that they would have lost I think up to 90 percent of the people they saved. What do you think? I mean, are we missing ---

MONTO: I think we've seen this in the United States, as well. It hasn't, because of the focal nature of the outbreak and our being a much bigger and more diverse country, we don't see the reports, as was in the Australian media of cases being --- when the ICU is overwhelmed and Carron's there flying the patient someplace else for care.

And I think Lori has made a very important point, though, about the parts of the world where these kinds of heroic measures are not possible. And that may explain what went on for a very brief time, actually, in the greater scheme of things, in Argentina, probably went on in Mexico, but that's kind of muddled because they were seeing other things being transmitted as well as the novel H1N1 virus.

But the concern is what we -- what is going on in the under- resourced countries -- and we may not even be hearing about it -- because, besides everything else in these under resource countries, they're used to having catastrophic events taking place without good surveillance systems and the rest and sub-Saharan Africa, we know very little about what's going on with influenza viruses in general. That's one of the targets for improvement in surveillance in that culture.

COHEN: Yeah, if you look at the map, it's not there.

MONTO: It's not there. It's sterile because you don't know about any viruses coming from there.

COHEN: We have a question that came in from the web from James Bailey: Why would we want people to get the swine flu vaccine and the seasonal flu vaccine? Wouldn't that in itself cause mixing in the human host and a potential for creating a new pandemic type virus?

SIMONSEN: No.

COHEN: Okay.

SIMONSEN: First of all ---

PALESE: If they're talking inactivated vaccines, no. If they're talking --

COHEN: --vaccines, killed virus, but the other one is live virus. So, inactivated, no, but could the live virus mix, do the two mix to create a new strain? Dr. Palese you've actually helped develop that vaccine. What do you think?

PALESE: I would like to say with great difficulty. I think this is very unlikely to happen.

SIMONSEN: And the only place that it's even a remote possibility would be someone who got the two live attenuated versions of the two vaccines at the same time.

COHEN: Which you're not supposed to do.

SIMONSEN: Yeah.

PALESE: Which you're not supposed to do.

COHEN: Right.

PALESE: Don't take antivirals at the same time because then you won't get infected by the live virus.

COHEN: Let's go to the far rear and then we'll come back to the center.

QUESTIONER: Good morning. Rory Lanceman. I'm a member of the New York State Assembly. We had a 12-hour hearing on H1N1 earlier this week and much of it focused on the mandatory vaccination that the New York state Department of Health has ordered of almost all health care workers in New York state and I was wondering if you could offer an opinion on whether you think such a policy is effective and sound.

MONTO: I have a very strong opinion about it. (Laughter.) And that is I think that's appropriate and I think it ties into a dilemma we're currently having about personal protective equipment and the way health care workers can be prevented from getting H1N1 influenza from their patients and also, the more likely event, transmitting H1N1 infections to their patients because, really, I think the debate about personal protective equipment -- availability of N95 masks -- is a fascinating discussion based on very little scientific evidence so that what you have is sort of inflated in terms of its value.

But the point I keep making is that you're more likely -- a health-care worker is more likely to get influenza from his or her children than from a patient in terms of protection of the health care worker, but even more importantly, because of this, is more likely to be able to transmit to another sick patient than anything else. And this is really what we're getting at, not so much protecting the health-care worker but protecting the patient indirectly because often these are immunodeficient patients and the rest who wouldn't benefit that much from vaccination.

COHEN: And I suppose you wouldn't even be having the debate if health care workers were first in line to get the vaccine, but that's part of the issue, right, is that ---

MONTO: Well, they are first in line to get the ---

COHEN: Well, they're given priority but do they --

MONTO: They're given priority but whether they're going to do it is another issue.

COHEN: Right.

PALESE: That recommendation, really, I think, makes a lot of sense based on scientific evidence.

COHEN: Then should we mandate for children?

(Laughter.)

COHEN: We do for school entry. Individual states do for school entry. Why don't we do that to protect the population? And we know that protecting our children from the vaccine, if they are indeed ten times more infectious ---

MONTO: A very brief answer which covers a lot of problems with influenza vaccine and we've heard it brought up already and that is, a lot of our problems with mandating influenza vaccine, use of influenza vaccine, would go away if we didn't have the need for annual vaccination. I mean, we've got a different kind of vaccine here, and I think we need to recognize the difference between influenza vaccine the way it's used and the fact that it's a good vaccine.

It's not a great vaccine. We've shown in a recent study 70 percent efficacy of the live vaccine in healthy adults young adults, who should have the best efficacy. We need, as we've heard, a better vaccine.

COHEN: Well, it's an interesting question, though. Would you be against mandating?

SIMONSEN: Well, I think this is very interesting because, I mean, especially for the health-care worker example. I mean, there are many, many good reasons why health care workers should be considering immunization for their own safety but also to protect and, first, do no harm to the patients that they are treating. Having said that, does it work to mandate?

I think what would work better would be to say that there was a shortage and people tend to buy more of something that's in demand. (Laughter.) We saw that -- there was one season where, really, people lined up all night to get a flu shot.

COHEN: Right.

SIMONSEN: And I mean ---

COHEN: Well, there is shortage.

SIMONSEN: No, actually, because we thought we were going to need two doses for every adult and since we are - only one dose, so, actually, we have twice as many doses and enough for the whole population at this point, I understand.

COHEN: But it's not there today, so --

SIMONSEN: Right, right. But I mean, that's --

COHEN: You had a question. You've been waiting a long time. And please identify yourself.

QUESTIONER: Alice Wong from Cal Tech. My question relates to the CDC updates and in their reports of isolates from throughout the world, Africa stands out as a continent that has more isolates of the regular annual flu than the other continents. They also do have isolates of 2009 H1N1. Do you think that the data are telling us something or that it is a result of bias in sampling or in reporting?

PALESE: I mean, I don't think it's bias and bad reporting. I think there are regional differences, and whether it really tells us something I'm not sure at this point. I know the data are mostly from South Africa, as I understand it.

PALESE: I'm not sure whether at this point it really tells us a lot, other than that there are differences. As you know, in New Zealand, for example, it's just the opposite. It's mostly 2009, H1N1. Maybe you're already sort of sensing something interesting going on, but I am not sure that it's, at this point, really clear what it means.

MONTO: But it does tell us we'd better use seasonal vaccine because the other viruses haven't gone away.

SIMONSEN: Right. It really goes to that bigger question -- will the other seasonal types come back in the winter and cause the usual epidemic that will kill a lot more elderly people? And, well, personally, I think that's a really interesting observation. I keep my eyes peeled on that kind of thing because if it exists anywhere on the globe it has the potential to come anywhere because, as we know now from understanding better the molecular epidemiology influence, it always comes by import.

It seems to come from the tropics and then every season you will see it, so as long as it exists in Africa and those South African -- (inaudible) --- surveillance systems, but there was also a false alarm from Egypt. Suddenly, we got some reports that there was a co- infection of H5 and H1 in a patient, and that turned out to not be true.

COHEN: We unfortunately only have time for one more question, so somebody go ahead in the rear.

QUESTIONER: Jim Shind from Princeton University. Some people have suggested that the swine flu experience was kind of a fortunate, if tragic because of the deaths, sort of a fortunate warm-up act for the real avian influenza doomsday scenario down the road. Do you concur with that and, if so, what do you think were the most important lessons that came out of the swine flu experience that are particularly important maybe in preparing us for the avian flu?

COHEN: I didn't plant the question, but it's perfect. It's a great wrap-up. What do you think? What have we learned from this teachable moment?

MONTO: I'll say something very brief and then give over to Peter, who I know has some strong opinions about the likelihood of an H5 pandemic and that is that talking with some of the local folks who had prepared, they thought, for an H5N1 pandemic, they felt that they were stressed by this in terms particularly of the surge for pediatric beds. There's not enough pediatric ICU beds so that I think this was a wakeup call in terms of preparing for something which would have different characteristics.

I'm not going to say more severe, less severe, and I think this is a -- this really was in some ways, and I take exactly what you were saying about it's too bad, but this really helps us in preparing. And I just want to remind everybody that there were only ten years or so between '57 and '68, 11 years, and these were bona fide pandemics without anybody debating was it a new sub-type or not a new sub-type, so we really can't anticipate anything in terms of how long we won't have another pandemic.

COHEN: Peter, briefly.

PALESE: Yeah, I think in a way even the H5N1, the avian threat ten years ago, prepared us for the current 2009 H1N1 outbreak, and I think if a new, real pandemic or a new strain emerges in the future I think it will help us to be prepared in a better way, so I think it also helps us to focus on the regular seasonal influenza, which I think is not being treated well enough in terms of preventing and in terms of a preparedness plan. So I think all of that helps us to get in better shape for future and seasonal influenza.

SIMONSEN: I think maybe this -- one focus that has come out of this particular experience is the focus and search, how important it is to understand the peak performance of a system. For example, in New Zealand, where they got so close to their capacity in the intensive care units, that's really an important thing to be aware of.

It really comes down to when the rubber hits the road, we now understand it's the hospitals we need to -- they need to really be prepared. Did they buy all the gloves and masks and what about the TB patients who now there's no more masks when we treat them. That's kind of where the action was at.

I had one meeting about that, about how, really, when you come from the perspective of the people who are going to treat the patients, that's really where the preparation is needed big time and that's the experience that has been had here.

COHEN: Well, I want to thank the panelists and all of you for coming and all of you for watching on the web. We're going to take a 15-minute break. Please return promptly because the next panel will start on time. Thank you all very much. (Applause.)

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