Here are answers to questions send to virology blog about the new strain of influenza H1N1 that is spreading globally.
Q: Regarding this marker (PB1-F2) – is it something that was present as well in the early wave of the 1918 virus, which was also considered mild up until August, or was it something that was acquired during its passage through humans? Do the steps being currently taken reduce the likelihood of sufficient human-to-human transmission to adapt and become more virulent?
A: It’s a good question. The 1918 sequences were obtained from autopsy material collected in September and November of 1918. Therefore we
can’t address the question of whether any changes occurred during propagation in humans. We can reduce but not eliminate transmission; therefore selection for viruses of greater virulence is still possible.
Q: Thank you very much for sharing with us the interview done to Ruben Donis. It is very provocative so I have several questions.
1. Has he uploaded to NCBI the sequence of the ninth virus that was not identical to those isolated in US? If not, Do you have any explanation for keeping secret this information.
A: Most of the sequences from Mexican isolates have been uploaded to GISAID.
2. He explains how it can be created new viruses by taking advantage of viral modules to make reassortments and the use of ferrets to check for pathogenicity. If by accident release infected ferrets into the wild, wouldn´t this a way to generate a new epidemic? If not, please explain.
A: Not necessarily. The particular combination of genes might not survive in the wild – for example they might not transmit well. But this is why these experiments are done under high containment.
3. Please explain Donis saying, and quote “the hemagglutinins we are seeing in this strain are a lonely branch” end of quote. Wouldn´t be this the reason for the higher pathogenicity of the viruses straines found in Mexico?
A: I assume he means that there aren’t many viruses with HA related to these strains. This observation makes no implications about pathogenicity. In any case all the strains appear to be on the same lonely branch.
Q: It would be very informative to know the origin of the specific H1 (and other) genes- avian or swine; it is unlikely that the H1 gene is from a current H1N1 human virus because it would be too similar to previous human H1N1 influenza viruses to presumably cause a pandemic.
A: Eurosurveillance has an article on bioinformatic analysis of the H1N1 sequences. They report: “Six segments of the virus are related to swine viruses from North America and the other two (NA and M) from swine viruses isolated in Europe/Asia. The closest clusters (for the HA segment) in the NCBI data base are North America swine influenza A(H1N2) and H3N2s. The closest relatives of the neuraminidase (NA) gene of the new virus, are influenza A isolates from 1992. The North American ancestors are related to the multiple reassortants, H1N2 and H3N2 swine viruses isolated in North America since 1998. In particular, the swine H3N2 isolates from 1998 were a triple reassortment of human, swine and avian origin.”
Q: After reading these news that a man seemingly infected pigs with flu on a farm in Canada, don’t you think that we should reconsider following pigs with more caution, I think that if this was true that pigs could catch the virus from humans, they could act as “Transit” station for re-emergence of the virus again and again, I don’t know if I am experiencing my mind well here, I mean given that pigs show mild or no symptoms at all, and that now they could acquire the virus from man, a farmer could give the pigs the virus and then leave the rest for the pigs to re-transmit the virus for other people, which in turn could transmit to other people and so on. This was a thought that I want to here what do you think.
A: The infection of Canadian pigs by a human with influenza returning from Mexico is disturbing, but there are many questions, elucidated in a previous post here. In short, it is incredible that such contamination was allowed to occur. Clearly pig-human interactions need to be carefully monitored. Culling herds should only be done when there is a known risk for spread of infection.
Q: I’m a bit confused: is it H1N1 or H3N2 from Eurasian pig flu virus? And does it directly copy it’s own RNA genome with the viral RNA polymerase?
A: NA and M genes are from Eurasian pig influenza virus. And yes, the viral RNAs are copied directly by the viral RNA polymerase.
Three related questions:
Q: How long would you expect human immunity to exist within an individual infected with h1n1 virus? I had the swine flu in the mid 70’s. Am I immune? Does getting H1N1 confer immunity in the future, and if so, for how long?
A: Natural infection confers lifelong immunity, but only to the infecting strain, not one that has drifted antigenically. As far as being infected by swine flu in the mid 1970s – this probably will not confer protection as the HA and NA of the two viruses are quite different.
Q: Are you aware of research out of the Kobe University Center for Infectious Diseases that more than 10% of pigs in Indonesia carry H5N1? Does this change your level of concern regarding the possibility of a recombination?
A: I haven’t seen that study published yet. But if it’s correct then of course there will be more concern about recombination. The more H5N1 replicates in pigs, the greater the chance.
Q: This may not be the best place to post this, but I find no other mention of it. There was an interesting ProMed-mail post today. Basically, the author, from the British Columbia Centre for Disease Control, says that while testing for H1N1, a lot of new cases of H3N2 were found, and that the H3N2 strain had changed. The author speculated that some of the late season Mexico flu reports could have actually been due to the new H3N2 variant.
A: It’s not surprising that H3N2 viruses are continuing to change as they circulate. What remains to be seen if they disappear with continued circulation of the new H1N1 strains. We won’t know the answer to this question for some time, and continued surveillance will be needed. A very interesting time for influenza virology.
Keep your questions coming to virology@virology.ws – I enjoy answering them.
we should all be knowledgeable about swine flu most especially on preventing it. we'll just hope and pray that this will end soon. it really affects the people, the education, lifestyle, economy, emotional state of the people.
You are a geek candy store. Thanks! The illustrations really help. I might need to explain some of this to some parents, so I'll do my best.
Are you aware of efforts to make the virus strain nomenclature more informative? Understanding what segments/genes are related historically and sequence wise to what is confusing using the 'serological' definitions like H1N1. What about the other segments? What about subtyping further the HA and NA genes?
Is there a good way to get a statistical handle on the relative rates if H1N1 isolate detection vs. others currently, particularly coinfection? Related to a question above, it will be interesting to see what happens with the flu species population and what the interaction of H1N1 in the background of other species will be.
Hello, first time poster but I've been reading this blog for some time now. This may have been discussed here before but I have a very simple question. The new H1N1 strain – does this represent antigenic drift or shift?
Many thanks!
What a good question, which no one has asked yet. Technically it is
shift because the new virus has a very different HA and NA from the
current circulating strains. But it's odd, because one of the current
strains is H1N1. But it's certainly not drift….this is defined as
small changes in the HA and/or NA that lead to slight immune evasion.
The new H1N1 could not have been derived from the previous H1N1 by a
few mutations.
Thanks, this is what is so interesting about influenza. Here we have a true antigenic shift – yet we may have seen more morbidity and mortality with a drift that would change the viruses’ virulence.
I think so many of us were expecting shift to represent a new HA (for humans) thus the dooms day scenarios. Thanks again and please, please, please keep this blog going!
my 11 year old Grandaughter has asthma and type 1 diabetes. three weeks ago she got sick and tested positive for influenzaA and negative for B. She was put on Tamiflu, increased asthma meds and her blood glucose went wild but now she is fine. my understanding is that she now has immunity to the strain she was infected with. my question is what are her chances at having some or complete immunity to strains that might evolve off the one she had?
If your granddaughter was infected with the 2009 H1N1 strain, then
there is a good chance that she'll be immune to the virus that
circulates in the fall. And if she is not completely immune, the
infection should be much less severe.
If your granddaughter was infected with the 2009 H1N1 strain, then
there is a good chance that she'll be immune to the virus that
circulates in the fall. And if she is not completely immune, the
infection should be much less severe.