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Tapping Minnesota’s top H1N1 expert: Michael Osterholm

As the saying goes, it's hard to be a prophet in your own hometown. So perhaps that's why some Minnesotans are unaware that one of the world's authorities on the novel H1N1 virus is one of our own. Michael Osterholm, PhD, is the head of the University of Minnesota's Center for Infectious Disease Research and Policy (CIDRAP). I spoke with him about the hard-charging H1N1 influenza virus.
On Monday the USDA confirmed that several pigs at the Minnesota State Fair were infected with the novel H1N1 virus by human fair-goers. Given the fact that H1N1 is already spreading easily from human-to-human, isn't this bigger news to the pork industry than it is to people?

"Well, it is and it isn't," Osterholm explained. "It is news to the pork industry in the sense that they're worried about any more bad publicity, given how hard the market has been hit, and we surely understand that. Countries around the world will use any excuse they can to use trade barriers, and everyone was concerned that, in fact, this would be another example of an inappropriate application of a trade barrier."

He pointed out that the Russians and Chinese, who already have trade barriers against pork imports, appear to be using this news to further support those trade barriers. "So from the standpoint of the pork industry, they have every reason to be concerned," he said. Osterholm continued by conscientiously reiterating what anyone with a pulse should know by now: You can't catch H1N1 from eating pork.

So yes, this is more bad publicity for the pork industry, but the news of the novel H1N1 being transmitted from humans to swine didn't come as a surprise to Osterholm. "We surely expected this, that this was going to happen, and we're going to see it in poultry, too. In fact, there's an outbreak [in poultry] in Ontario right now and there's going to be more." A recently recognized human-to-swine transmission in Australia generated the memorable sentence, "A piggery near Toowoomba has been placed under quarantine…."

Dr. Michael Osterholm
Dr. Michael Osterholm

So the novel H1N1 virus, already an assortment of swine, human and avian influenza strains, is going back to the well. Is there any danger that it could re-emerge with new powers?
"This has not received a lot of attention, but there is legitimate concern about the virus's getting back into pigs, reassorting with other swine influenza viruses, and then coming back out again," Osterholm said.

Now, can anyone tell you how often that happens? "No," he flatly admitted. As he pointed out, although swine have historically been a prime melting pot for influenza viruses, they are not essential to the process. The billion or more humans who will become infected with H1N1 will provide the virus with plenty of chances to reshuffle its genetic deck.
"I think there's been the suggestion that the virus will only change if it goes back into pigs," Osterholm told me. "No, it's just one more source of where a change could occur. It could surely mutate or even reassort in humans. You can have humans infected with two viruses at once — that's not unlikely at all." And when two different viruses are infecting the same cell, that's where the genetic swap meet can begin.
We speak of flu viruses as being either human, or swine, or avian, but like the novel H1N1 virus, aren't all influenza viruses really mutts?
"That's the key piece: They are mutts, and we don't really know what are the component pieces that are going to make that mutt special," he said.

Osterholm chairs a National Institutes of Health (NIH)-sponsored panel that tracks emerging influenza infections. This year's meeting included a group of virologists and influenza experts that Osterholm considers to be the best in the world. "And every one of them said without a question that if this H1N1 acquires a certain PB2 gene, we're in big trouble," Osterholm recalled. "Well, it did it [acquire the PB2 gene] in the Friesian islands off of the Netherlands this August, and we didn't see that. Everyone was holding their breath, but at least, so far, nothing has happened with that. And so we don't understand in many instances what components of the mutt are really critical, which ones are important and which ones don't make any difference."
If a virus hits a winning combination for infecting a particular species (humans in this case), does that make it hard for the virus to go back and be really good at infecting other species? Has there ever been an influenza virus that hit the jackpot, having the ability to infect multiple species and cause severe illness?
"There's nothing in nature that would support that," he said, " and the reason for that is if the virus did that, it wouldn't have a reservoir or a host."

While having the ability to infect different species is in a virus's best interest, killing its host is not. Viruses want to propagate, not kill. The best situation for a virus is to find a host that continues to stay healthy even while infected. Pigs, for example, are a nice reservoir for influenza because they are typically asymptomatic. According to Osterholm, we now know that the dreaded Ebola virus finds its safe haven in certain bats that have asymptomatic infection, and for unclear reasons, the HIV virus causes much milder disease in subhuman primates than it does in humans.
At the MDH H1N1 Pandemic Summit held last month, you predicted the virus would arrive well before the vaccine. It looks like you're going to be right.
"Well, I wish I were wrong, but I have been concerned from the beginning about over-promising and under-delivering on this issue. Just knowing this vaccine and what it takes, when they put the 140 million-dose estimate out that would be here in mid-October, I just knew that that was going to be a great overreach. That's not a problem if the public doesn't hang on it. But we're sending such mixed messages to the public."
By mixed messages, he means pushing the public hard about the importance of getting vaccinated, thereby creating a demand for a product that has yet to materialize.
"Go to '' and they have a flu vaccine locator sitting right in the front page. You go to that and it's a dead end everywhere you go. And that's because there is no place that has vaccine. When I say 'no place,' it's coming out in dribbles," Osterholm told me. "I'm hearing from more and more medical offices that are really upset because they're having major problems right now with so many people calling in for vaccine that it's beginning to compromise their reception lines. They can't get really sick people to get through."
Do you have a sense where the hang-up is in the current vaccine production?

"It's a lot like planting corn in Iowa: You can't harvest until it is ready to go. They were predicting 'if we did early silage, what could we get?' versus 'what could we get if we had to pick it when it was dried and ready to go?' " Osterholm explained. "It's not hung up on anything that is administrative or a mess-up; it just takes this long. I'm not the only one that just said, 'That time line is not realistic.' And so I'm not surprised, and I find no fault at all — in fact I find it remarkable that we have as much as we do as early as we do, given the timeline. Like I said, any time you have a vaccine now that literally takes as long to make as it does to plant and harvest corn in Iowa, then you know you've got a problem with your vaccine."
Long before the arrival of the novel H1N1 virus, Osterholm and other infectious disease specialists were lamenting our country's antiquated vaccine production system, which he points out relies on 1950s technology that's slow and unreliable. And even the way in which influenza vaccines work is a little bit murky.
"On Monday, I'm giving the keynote address to the NIH vaccine research meeting," he said. "I'm actually using H1N1 to highlight the many problems we have today with the vaccine industry.  It's a simple as, 'You know, we don't have a clue what protects you in a flu vaccine.' So we measure hemagglutinin [the 'H' in H1N1] using outdated measures for antigen [a molecule on the surface of a virus that our immune system uses to key in on it], but we don't really know."
There are two basic ways to destroy an infection: with antibodies, which act as bullets, or by what's termed "cellular immunity," wherein certain white blood cells identify, engulf and kill the virus. Current testing involves only antibody testing, which, as Osterholm explains, doesn't leave us with a good sense of how effective and protective a vaccine might be.
"When the CDC did their sero-survey looking for hemagglutinin antibody to novel H1N1 in the elderly, they found about 30 percent of them having pretty good titers to the H1 N1 virus," Osterholm recalled. "But the bottom line is, the protection we're seeing in the 65 and older age population far exceeds 30 percent, and the point of it is that there is probably a huge part of cellular immunity that's tied to protection with the flu vaccine, and that's something we don't even understand."
"So it's something as simple as people think we know what it is in the flu vaccine that protects you, that we don't even really know. I can give you a whole laundry list of things people would be surprised at," Osterholm said. "The one thing I do feel pretty good about is the safety issue. It's not because we know it from this vaccine, but from the time-tested seasonal flu vaccines we've used over the last 30 years."
So the vaccine will get here when it gets here, but do you have a sense of when the peak of infections will be?
"You know, I don't. As I said at the flu summit six weeks ago, I thought that by mid-October we'd be seeing what I call 'peak activity,' which is what we're seeing right now. That's how I thought it would build. What I don't know is how long this is going to last. Is it basically going to go into retreat for a while and then come back again in, say, December or January? We're burning through a lot of central people right now, meaning the rate of new infections is growing at such a rate that I think that we're not going to have that many [unexposed] people left in November, December or January to get a second wave. But I don't know that — we'll have to see. I think right now, if it continues to build like this, that could be the peak for the year."
Do you have any idea what percentage of the population will end up getting infected?
"I can't say it's old wives' tales, but it's kind of that situation," Osterholm said. "We often talk about a third to 50 percent of the population will get it, but again, remember, with a new strain like this, and the age-related immunity [in those people older than 65], it could very well be as high as 60 to 70 percent for some age groups, and it could be as low as 20 percent for others."
I kidded Osterholm that for a man who knows so much about influenza, he sure does say, "We really don't know" a lot. 
"I know less today than I did 10 years ago!" Osterholm said, laughing. By "less," he means to say that an answer to one question seems to raise five new ones.

"The more we've learned about these viruses, and the more challenges that we come up with, the more I realize, 'Here's a vaccine produced with 1950s technology; we're using outdated ways to measure the way it protects; we don't have a good way to make it in a timely way,' " Osterholm said. As he describes it, the novel H1N1 virus continues to both fascinate and humble those who study it.
"If you had presented this virus to us four months before the first jump to humans, I don't think there is any way anybody could have told you, 'This is the next pandemic strain.' Sometimes we just have to honest about that and say, 'Sure we'd like more data, we'd like to understand these better, and one day wouldn't it be great if we could, like a Pap smear [which grades the risk of progression to cervical cancer], tell you we're on the path here to a pandemic strain, and if this continues to change, and these changes occur, this could be then next pandemic strain.

"But we're so far from that. I mean, we're going to solve global climate change probably before we solve that one."

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Comments (3)

This has been one time when I have been very disappointed in our authorities and/or government. The analogies made to identification and production here have helped shed some light. It seemed to me (just a regular guy) the outbreak last Spring gave enough lead time but of course viruses mutate and I didn't know the production time was so lengthy. It seems we could have spent 2-3 times as much, put it on an emergency footing even if wasteful and gotten better results it would have been money well spent.
Once again Dr. keep writing this column often as I do find it reassuring coming directly from you and not a journalist. Thanks so much.

Osterholm has been labeled a fear-monger by his detractors. Not so. I would submit that he has attempted what, in this generation, is a novel thing, i.e., telling the truth that is rooted in factual data. We would be well-advised to listen up.

I agree with you Barbara. Talking realistically and factually about fearful things does not make one a fear-monger.