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PLoS Comp. Bio.: Spring & Early Summer Most Likely Time For A Pandemic

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  • PLoS Comp. Bio.: Spring & Early Summer Most Likely Time For A Pandemic

    PLoS Comp. Bio.: Spring & Early Summer Most Likely Time For A Pandemic

    Credit Spencer J. Fox
    #12,842


    We've a new study, just published in PLoS Computational Biology, that looks at the history of 6 pandemics in the Northern Hemisphere since 1889, and finds they all first emerged in spring and early summer. Using a computer model, the authors found evidence of a narrow window of opportunity for pandemic emergence.
    The authors then proposed two possible factors behind this trend, one of which long time readers of this blog will recall was a frequent topic of conversation after the last pandemic.
    First some excerpts from a press release from the University of Texas At Austin, and a link and some excerpts from the study, then I'll return with a jaunt down memory lane.
    You might expect that the risk of a new flu pandemic ? or worldwide disease outbreak ? is greatest at the peak of the flu season in winter, when viruses are most abundant and most likely to spread. Instead, all six flu pandemics that have occurred since 1889 emerged in spring and summer months. And that got some University of Texas at Austin scientists wondering, why is that?

    Based on their computational model that mimics viral spread during flu season, graduate student Spencer Fox and his colleagues found strong evidence that the late timing of flu pandemics is caused by two opposing factors: Flu spreads best under winter environmental and social conditions. However, people who are infected by one flu virus can develop temporary immune protection against other flu viruses, slowing potential pandemics. Together, this leaves a narrow window toward the end of the flu season for new pandemics to emerge.

    The researchers? model assumes that people infected with seasonal flu gain long-term immunity to seasonal flu and short-term immunity to emerging pandemic viruses. The model incorporates data on flu transmission from the 2008-2009 flu season and correctly predicted the timing of the 2009 H1N1 pandemic.
    (Continue . . . )


    Seasonality in risk of pandemic influenza emergence

    Spencer J. Fox , Joel C. Miller, Lauren Ancel Meyers

    Published: October 19, 2017
    Author summary Influenza pandemics emerge via genomic reassortment between circulating human and animal strains. The risk of pandemic emergence should therefore be high during the flu season, when viruses are abundant and conditions favor transmission. However, the six pandemics on record since 1889 all emerged in the Northern Hemisphere following the flu season, suggesting that other forces may predictably constrain pandemic risk. We find that seasonal influenza epidemics leave a wake of immunity that impedes pandemic emergence. This transient refractory period is consistent with the spring-summer emergence, multiple wave dynamics of recent pandemics, and may cause initial underestimation of the viral transmission rate. These findings may improve pre-pandemic risk assessments and real-time situational awareness, particularly as we gain greater insight into the extent of immunity.


    Abstract

    Influenza pandemics can emerge unexpectedly and wreak global devastation. However, each of the six pandemics since 1889 emerged in the Northern Hemisphere just after the flu season, suggesting that pandemic timing may be predictable.
    Using a stochastic model fit to seasonal flu surveillance data from the United States, we find that seasonal flu leaves a transient wake of heterosubtypic immunity that impedes the emergence of novel flu viruses. This refractory period provides a simple explanation for not only the spring-summer timing of historical pandemics, but also early increases in pandemic severity and multiple waves of transmission.
    Thus, pandemic risk may be seasonal and predictable, with the accuracy of pre-pandemic and real-time risk assessments hinging on reliable seasonal influenza surveillance and precise estimates of the breadth and duration of heterosubtypic immunity.
    (Continue . . )



    Eight years ago, months after the 2009 H1N1 pandemic had emerged - but a couple of months before the monovalent H1N1 vaccine would be available - news of an unpublished Canadian study began to surface that suggested that those who had received a seasonal flu shot the previous year were more likely to contract the new pandemic virus than those who hadn?t.
    Helen Branswell, science and medical reporter for the Canadian Press, was among the first to report on it (see Branswell On The Canadian Flu Shot Controversy).
    The CDC and the World Health Organization both looked at their data, and issued statements that they could find no correlation between the seasonal vaccination and increased susceptibility to the pandemic flu.

    With concerns rising, a number of Canadian Provinces halted or announced delays in rolling out the seasonal flu shot, even though the study had yet to be published (see Ontario Adjusts Vaccination Plan).
    The debate raged on, with conflicting data (see here, here, and here), long after the 2009 pandemic ended.
    In November of 2010, an article appeared in the Eurosurveillance Journal (see Eurosurveillance: The Temporary Immunity Hypothesis) that suggested that contracting seasonal flu (as opposed to being vaccinated against it) temporarily ramped up the body?s immune system against other viruses ? and that this protective effect could last months.
    Eurosurveillance, Volume 15, Issue 47, 25 November 2010

    Perspectives
    Seasonal influenza vaccination and the risk of infection with pandemic influenza: a possible illustration of non-specific temporary immunity following infection

    H Kelly , S Barry, K Laurie, G Mercer
    Unlike the Canadian researchers, these scientists could find no increased susceptibility to the pandemic H1N1 virus among Australians who had been vaccinated the previous year against seasonal flu. The difference between the two findings, they posited, came from three separate factors:
    • A theory regarding temporary immunity following any influenza infection
    • The timing of the arrival of the pandemic virus in Canada
    • And the protective effects of seasonal flu vaccination against seasonal - but not pandemic - flu.

    While unproven, this hypothesis fits in nicely with the findings of today's study.
    Dr. Ian Mackay discussed a similar hypothesis in his blog back in 2014, in Influenza in Queensland, Australia: 1-Jan (Week 1) to 8-June (Week 23), where he suggested that the immune response to the early spread of one respiratory virus might dampen the spread of a second virus - perhaps for months - what he dubbed a `shields up' effect.
    While there could be other factors we don't know about that might override this proposed narrow window of opportunity for pandemics - based on the historical record and the growing evidence for the temporary immunity hypothesis - late spring and early summer do seem the most likely time for pandemic emergence.


    http://afludiary.blogspot.com/2017/1...ly-summer.html
    Last edited by Michael Coston; October 20, 2017, 11:21 AM.
    All medical discussions are for educational purposes. I am not a doctor, just a retired paramedic. Nothing I post should be construed as specific medical advice. If you have a medical problem, see your physician.

  • #2
    I am dubious. It seems unlikely that the 10%ish/head annual flu burden would provide sufficient heard immunity to play a significant role in thwarting a nascent flu pandemic. It is difficult to see it providing an adequate counter force to the increased chance of reassortment, or recombination, provided by dual infection either between seasonal flu strains or a seasonal flu and some zoonotic strain in close contact with humans at the peak of the flu season.
    Last edited by JJackson; October 23, 2017, 11:53 AM.

    Comment


    • #3
      I share a certain amount of skepticism (I suspect that a sufficiently virulent and transmissilbe novel flu could emerge at any time of the year), but I assume this theory considers the full impact of winter respiratory virus impacts - not just influenza - in raising community immune responses.

      That said, we humans are extrodinarily good at seeing patterns in limited data sets that turn out not to hold true over the long run. So while an interesting and seemingly elegant theory, I wouldn't wager any money on it.
      All medical discussions are for educational purposes. I am not a doctor, just a retired paramedic. Nothing I post should be construed as specific medical advice. If you have a medical problem, see your physician.

      Comment


      • #4
        I assume this theory considers the full impact of winter respiratory virus impacts - not just influenza - in raising community immune responses.
        How would you see it doing that? Is there evidence of an acquired immunity derived from anything but flu, or were you thinking of heightened innate response due to greater general challenge during the winter months? Apart from colds & flu what other diseases show a marked seasonality (apart from vector borne)?
        Mike, sorry about all the question, you just got me wondering.

        Comment


        • #5
          With the understanding that we dealing with OPHs (Other People's Hypotheses), a couple of references . . .

          The Temporary Immunity Hypothesis posited in the 2010 Eurosurveillance article ( http://www.eurosurveillance.org/cont...15.47.19722-en )
          The temporary immunity hypothesis
          We would like to suggest an alternative hypothesis to explain the findings from both Canada and Victoria. In our hypothesis recent infection with any strain of influenza would confer temporary immunity to infection with any other strain, independent of antigenic distance, but vaccination would not confer protection unless the vaccine and circulating strains were antigenically similar.

          (SNIP)

          Extending this hypothesis, and further suggesting that temporary immunity may be conferred not only by influenza infections but also by other viral infections, is a contemporary report from Sweden that rhinovirus infection may have decreased the risk of infection with pandemic influenza A(H1N1) by what was suggested to be a cytokine-mediated phenomenon [24].
          In 2014, Ian Mckay wrote in his blog (https://virologydownunder.blogspot.c...lia-1-jan.html) about his own hypothesis:


          When there are enough of us in the community infected by one virus (say respiratory syncytial virus [RSV]) and our immune-thing-a-me-whats-it is all fired up and producing an inflammatory response to rid us off said pestilence, that responsey thing offers a kind of "Shield's Up" effect.

          For a short while we feel like rubbish but we also don't let other viruses get in as easily because we're in an "antiviral state". Enough of us in that state and we get a kind of short-term herd immunity (a fairy died) - where the number of people fully susceptible to another virus (say, an influenza virus) is too small for it to get a good toehold in us and the population. This pattern among seasonal respiratory viruses is most often observed, in my experience, for viruses with an RNA genome like RSV, rhinoviruses and influenza viruses.
          I'm sure a deeper search would turn up more, but how much merit there is to all of this is way above my paygrade. Hope this helps.
          All medical discussions are for educational purposes. I am not a doctor, just a retired paramedic. Nothing I post should be construed as specific medical advice. If you have a medical problem, see your physician.

          Comment


          • #6
            Many thanks. I am averse to theories I can not see a mechanism for, but these make some sense. The bit before the SNIP would be acquired caused by one or more of the antigenic sites on HA or NA leading to matched memory T-cells releasing cytokines that would accelerate a response. The bit about but 'not with a vaccine' I do not get as current vaccines should, in theory, elicit the same response, but to a lesser degree than a full-blown infection. After the SNIP and the bottom box would be the 'heightened innate response' guessed at earlier which I assume to be minor unless soon after previous infection. I tend to think of all of these things in terms of the resultant force vector from many individual force pushing in different directions to different degrees but trying to assign values to all these vectors to achieve a quantitative, rather than qualitative, resultant force is also way above my paygrade. I was concerned that there may have been an important piece of the puzzle that I was unaware of.

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