CDC, Press briefing transcripts, May 7, 2009, 4 PM ET, New England Journal of Medicine Articles on H1N1 Flu, 1918 flu pandemic, H1N1 Virus, Triple Reassortant Swine Influenza A (H1)

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“Press Briefing Transcripts

CDC Telebriefing on New England Journal of Medicine Articles on H1N1 Flu

May 7, 2009, 4 p.m. ET”

“>>> Welcome and thank you for standing by.  At this time, all participants are in listen-only mode until the question and answer period of today’s conference call.  During the question and answer session, you may press star one to ask a question.  At this time, I’ll turn the call Over to Mr. Dave Daigle.  You may begin. 

>> Hi, this is Dave Daigle, with CDC Media Relations, thank you for joining us on this short-notice telebriefing to discuss two “New England Journal of Medicine” publications: The Emergence of Novel Swine-Origin Influenza A H1N1 Virus in Humans and Human Infections with Triple-Reassortant Swine Influenza A (H1) in the U.S. from 2005 to 2009.  Joining us today are Drs. Michael Shaw, Lyn Finelli, Carolyn Bridges and Fatimah Dawood. I think we’re going dispense with opening statements and just go right into the questions.  So can we have the first question, please? 

>> Thank you, again. If you would like to ask a question, please press star one.  Our first question comes today from Donald McNeil with “The New York Times.” You may ask your question. 

>> Hi.  In reading over the article about the triple-reassortant swine influenza A. I’m assuming this is tracing infections that do not include the Eurasian swine sequence found in the patients in the current outbreak, and I wondered if you can tell us more about whether or not that Eurasian swine strain had ever been found in the United States, whether you can tell from genetic sequencing where it got into the combination along with these triple reassortants or give us any details of that.

>> Those genes had never been seen in the Americas before. 

>> Wait one second, this is Dr. Michael Shaw.

>> Thank you.

>> This was the first time they had been seen in any virus in any human or animal.  And the genetic lineage of the virus we can trace back, there’s clearly a gap in the surveillance because there are no really close relatives, nothing that we can say was an immediate precursor.  Because of this new finding, a lot of researchers in the field are going back through their archives now, digging through their freezers to see if they had something that was overlooked but there’s absolutely nothing in the literature, nothing publicly available and nothing that our colleagues knew about when this was first found. 

>> This is Carolyn Bridges.  I think it’s also important maybe to just point out and maybe you want to take questions over to USDA as well, but from our understanding, there were no importation of pigs into the United States from Eurasia.

>> Next question, please.

>> Our next question comes from Maggie Fox with Reuters. 

>> Oh, darn, I wanted someone else to ask some first.  Can we go back over that, what is it that’s new and any hint as to whether somebody might have carried this reassortant to Mexico or whether it emerged there considering the surveillance we have is of people who had that triple-reassortant in the U.S. 

>> This is Michael Shaw again.  Genetics are indicating that the origin of this virus apparently happened before anyone was aware of it occurring in animals or humans.  It was six of the genes were similar to what had already been seen in the Americas circulating in pigs and that we knew about.  The acquisition of these two new Genes from the Eurasian lineage have never been seen in the Americas.  There is importation of pigs, the way I understand, too to Europe and Asia for breeding purposes, but not the other way around.  So whether it might have come into this hemisphere by a person or an animal, we have no idea.  There’s just not — we’re not in a position to say right now. 

>> Thank you, Maggie.  Next question, please.

>> Thank you, our next question comes from Mike Stope from Associated Press.  Ask your question. 

>> Hi, thanks, doctors, for doing this.  Two questions.  The first one, I saw in one of the articles, we saw this in I think the MMWR2, 38% of cases in the U.S. looking at the U.S. cases also involved vomiting or diarrhea.  That’s not typical of seasonal influenza.  What explains that in this virus?  Can you give us any information about what is it about this virus that’s causing those symptoms at a higher amount? 

>> Yes.  This is Fatimah Dawood.  We did find in the first 642 cases or patients who are diagnosed with swine-origin influenza virus infection that 25% either had diarrhea or vomiting.  This is a new virus and we’re still learning how transmission occurs.  But because we’ve made this observation, we are recommending that clinicians think about transmission not only through a respiratory route but also through the gastrointestinal route as fecal-oral transmission, but it’s not fully understood what role those symptoms played yet.

>> Thank you, Mike.  Next question, please. 

>> Thank you.  Our next question comes from Heidi Sloot with “Internal Medicine News.”  You may ask your question.

>> Hi.  Thanks for taking my question.  This is sort of a follow-up to the previous question.  What right now is the take-home message then for clinician relating to this as far as symptoms to watch for or what to tell patients? 

>> This is Fatimah Dawood again.  In our paper, again we looked at the first 642 cases and we found that the majority of people with confirmed swine-origin influenza virus infection had symptoms that are typical of seasonal influenza.  Those would include fever, cough and sore throat, which are the three most common symptoms observed.  As mentioned previously, diarrhea and vomiting were prominent symptoms as well, so what I would say is that clinicians and people should be aware of those symptoms and I think that as members of the community have symptoms that are concerning to them, they should discuss that with their clinician.

>> Thanks very much.  Next question, please.

>> Thank you, our next question comes from Daniel Denude with webmd.

>> Thanks for taking my question.  I have to push beyond this.  Perhaps you all noticed there was also a paper published at the same time about the signature features of pandemic flus in the past and it strikes me that these flus continually seem to have some of the features that we’re seeing here, striking younger people, and that there is a wave phenomenon.  I wonder if you could comment on the risk groups that you’re seeing for this virus and what we might expect looking forward from our experience with pandemic flu about what future waves of viruses tend to look like as they tend to become pandemic.  I know that’s a wide question but I appreciate you addressing it.

>> This is Fatimah Dawood.  You know, I would say that this is an evolving outbreak and we’re still learning about how this virus works, but what we observed in our paper is that 60% of confirmed cases occurred in people who are 18 years of age and younger.  Now there may be several possible explanations for that. One is the possibility that younger people are more susceptible to the virus, but there may also be a bias in the way that we are finding cases right now because the numbers of cases were identified in school outbreaks and still more young people are being tested right now.  There is also the possibility that older people may have some antibodies to other influenza viruses that give them cross protection against the current virus.  I think it’s difficult to make predictions at this point. 

>> This is Dr. Carolyn Bridges. In terms of the second part of your question about what we might expect, of course we’ll have to sort of wait and see, that’s always the tricky part with influenza.  We never sort of know what we’re going to get until we get there.  But with past pandemics where there’s been a novel strain where there has been initiation or introduction of that virus, the initial outbreaks if they occur in the summer are generally milder.  We know that the influenza virus, in general, prefers lower humidity, lower temperatures for transmission.  So as we’re in the summertime, we expect it to be seasonal influenza but what we’re likely to see is some transmission that occurs over the summer with the possibility that in the fall when the weather turns cooler again that we might see an increase in cases that will be looking closely toward the southern hemisphere, during their winter that is coming up to see what happens and that may give us some clues as to what we might expect in the upcoming winter months here in the United States.

>> Thank you very much.  Next question, please. 

>> Our next question comes from John Warren with Bloomberg News, you may ask your question.

>> Hi.  Thanks for taking my question.  Yeah, I was wondering if you could talk more about whether the ancestors of this virus may have been circulating in people before it was in pigs and whether that might have given immunity to older people.  Thanks.

>> This is Michael Shaw.  Well, ultimately all of the ancestors of this particular swine strain and circulating seasonal H1N1 can be traced back to the 1918 pandemic.  That virus established itself both in humans and in pigs.  And they’ve been evolving along separate tracks.  And in the process being both mammalian species they’ve maintained the ability to go back and forth, which is what we’ve seen obviously, for example, in the other paper we’re talking about today that they are able to make the jump.  What’s unusual about this particular case, is that it’s able to apparently establish sustained transmission.  What’s clear from what we’re seeing genetically and just the behavior of the virus, it was already well-adapted for transmission in humans before it popped up in this particular case.  But ancestors are the same.  You can trace them all back to 1918. 

>> Thank you, John.  Next question, please.

>> Thank you.  Our next question comes from Elizabeth Weiss with “USA Today.”  You may ask your question. 

>> Hi.  Thanks for taking my call.  This is follow-up on that then. You talked about there may be a missing link in observation or surveillance.  How much observation and surveillance is there worldwide and how likely is it that you would actually see something close to real-time virus like this popping up? 

>> This is Carolyn Bridges.  I think what we can say is that we certainly are much better prepared this year than we would have been a few years ago.  And although what we were preparing for most urgently was potential emergence and spread of H5N1, the avian virus, those investments have paid off in spades.  And so we have invested from the U.S. government with many colleagues from different countries.  Other donors in increasing laboratory capacity in countries around the world.  So I can’t tell you for sure how early we might be able to identify — have identified this virus, but we certainly are in much better shape than we would have been even just two years ago.

>> Thanks.  Next question, please.

>> Thank you, our next question comes from Mary Manning with “Las Vegas Sun.”  You may ask your question.

>> Yes.  Thank you for taking my question.  I’d like to know if there’s been any studies done on how long this virus lasts when it gets out in the environment? 

>> This is Michael Shaw.  There have been no — we haven’t had the virus long enough to do studies on this particular one.  All I can go by is past experience with other influenza viruses.  It depends on the environmental conditions.  It survives better on a hard surface than a porous surface, for example.  It’s inactivated quickly at higher temperatures.  Those are just general facts about flu.  But these particular strains, people are working on it.  We haven’t done — don’t have that information yet. 

>> Thanks very much.  Next question.

>> Thank you, our next question comes from Brian Thompson with KS public radio.  You may ask your question.

>> Hi.  Thanks for this opportunity.  As for the predecessors of this virus that emerged in pigs in the late 1990s, the humane society of the U.S. has made the argument that intensive factory farming is responsible for the shift in the genes that caused all this to happen.  I’d like you — Juergen Rick at Kansas State University, by the way ,argues that backyard pigs would be more susceptible because they are exposed to more viruses left by bird droppings and such.  So I would like you to weigh in on that, please. 

>> This is Carolyn Bridges.  I’m not sure we can really speculate about that, given what we believe based on the data that we have available from the genetic databases is that we don’t have any precursors like this in the United States despite tremendous amount of surveillance that goes on here in the U.S.  So I can’t speculate.  I wouldn’t able to say one way or the other. 

>> Thanks very much.  Next question.

>> Thank you.  Again, I’d like to invite parties who would like to ask a question, press star one.  Record your name prior to asking a question.  Our next question comes from Carrie Peyton with Sacramento Bee newspaper.  You may ask your question.

>> Hi.  Thanks for taking this question.  As we continue to do genetic analyses of these virus throughout the southern hemisphere flu season, what markers, if we start seeing changes in different markers, which ones would be especially troubling.  What areas of the genome do we not want to see change or would be early signs of it changing in ways that could make it much more prominent? 

>> This is Michael Shaw, there’s several critical parts of the genome that we look at.  Obviously the one primary concern right now is the determinants of resistance to the antiviral agents.  That’s going to be a high priority to continue monitoring.  Also any potential changes in the surface proteins that could potentially complicate selection of a vaccine strain.  As you know, under ordinary circumstances circulating influenza varies a great deal which is why the vaccine has to be updated every year.  There is the possibility that once it starts circulating more wide lane and different populations that you’re going to see, subpopulations popping up that could not be reactive with whatever vaccine strain might be chosen.  So we just have to keep an eye on changes in general, but the ones we look for in particular are the ones that are affecting the genetic makeup of the proteins that react with the vaccine and antiviral resistance or susceptibility.

>> Thanks very much.  Next question.

>> Thank you.  Our next question comes from Mike Shope with Associated Press.  You may ask your question.

>> Here’s the second question I was trying to ask earlier.  There’s a little bit more detail on the chronic conditions that the severe cases in the U.S., especially in the cases of the two deaths, the 22-month-old child had it looks like four conditions and a pregnant woman had several including autoimmune disease that was under treatment.  Can you tell me about those constellations of underlying conditions.  Would seasonal flu have killed those patients given those conditions?  Or are you learning anything about the patients who suffered severely who had underlying conditions?  What’s working together there? 

>> This is Fatimah Dawood.  I think we’re still learning about what patients are still most at risk for swine origin influenza virus and complication of that infection.  But what we do know from seasonal influenza is there are groups of people with characteristics with a higher risk.  That includes children younger than age 5, people with chronic underlying medical conditions.  Pregnant women and adults older than 65 years of a and one thing that we looked at in the 642 patients that were described in this paper and then in the subset of patients who were hospitalized, we had data for 22 patients.  About half of those patients had one of those characteristics.  Which does suggest that those groups of people may be at higher risk.  Those groups may not be the only groups but certainly we are seeing that those groups are well represented amongst the people who are hospitalized at this point. 

>> Thank you it, Mike.  Next question.

>> Thank you, our next question comes from Elizabeth Sweeth with “USA Today.”  You may ask your question.

>> Thanks again.  Just a quick question, I’m reading these paper, some of the facts are actually from May 5th.  I’m wondering when are these going to published and have you all ever done this quick a turnaround before I don’t recall having seen it.

>> This is Lyn.  I may be here the longest of anyone at this table.  I have never seen such a paper come out so quickly, I don’t think.  Is that what the question was? 

>> Right.  I mean there’s data in there from two days ago.  When I’m wondering when is it going to come out in print?  From your memories, some of the AIDS papers came out quickly, but quickly went three or four weeks.  I have never seen anything show up two days later.

>> I think print of both of these papers is going to come out the first week of July. 

>> This is Carolyn Bridges, but I understand these version are available online to anyone, not just by subscription, anyone would have access to these papers. 

>> This is Fatimah Dawood.  I would just add to that this paper is an effort by so many people in county and state health departments as well as CDC to really make this information available as soon as possible to people. 

>> Yeah, and this is Michael Shaw.  I want to emphasize we were getting this genetic information out basically as soon as we had it.  We had the first gene segments up there in April 25 and made special arrangements at NCBI and NIH to have them released essentially as they were submitted so.  April 27th, things started to getting up on the NIH, NCBI website right away as soon as we had the data.  There was no holding back of it.

>> Operator, this is Dave.  I think that was our last call.  So I want to thank everybody for taking the time to join us today to ask questions.  We’ll plan another daily update briefing tomorrow, regular CDC press briefing.  Thanks, everyone. 

>> Thank you.  At this time, that does end this conference.  All parties may disconnect. 




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