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Emergence and dynamics of influenza super-strains

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  • Emergence and dynamics of influenza super-strains

    BMC Public Health. 2011 Feb 25;11 Suppl 1:S6.
    Emergence and dynamics of influenza super-strains.

    Coburn BJ, Cosner C, Ruan S.

    Center for Biomedical Modeling, Semel Institute of Neuroscience & Human Behavior, David Geffen School of Medicine, University of California, Los Angeles, 10940 Wilshire Blvd, Suite 1450, Los Angeles, CA 90024, USA.

    ABSTRACT : BACKGROUND :Influenza super-strains can emerge through recombination of strains from birds, pigs, and humans. However, once a new recombinant strain emerges, it is not clear whether the strain is capable of sustaining an outbreak. In certain cases, such strains have caused major influenza pandemics. METHODS : Here we develop a multi-host (i.e., birds, pigs, and humans) and multi-strain model of influenza to analyze the outcome of emergent strains. In the model, pigs act as "mixing vessels" for avian and human strains and can produce super-strains from genetic recombination. RESULTS : We find that epidemiological outcomes are predicted by three factors: (i) contact between pigs and humans, (ii) transmissibility of the super-strain in humans, and (iii) transmissibility from pigs to humans. Specifically, outbreaks will reoccur when the super-strain intections are less frequent between humans (e.g., R0=1.4) but grequent from pigs to humans, and a large-scale outbreak followed by successively damping outbreaks will occur when human transmissibility is high (e.g., R0=2.3). The average time between the initial outbreak and the first resurgence varies from 41 to 82 years. We determine the largest outbreak will occur when 2.3 <R0 < 3.8 and the highest cumulative infections occur when 0 <R0 < 3.0 and is dependent on the frequency of pig-to-human infections for lower R0 values (0 <R0 < 1.9). <r0><r0><r0> CONCLUSIONS : Our results provide insights on the effect of species interactions on the dynamics of influenza super-strains. Counter intuitively, epidemics may occur in humans even if the transmissibility of a super-strain is low. Surprisingly, our modeling shows strains that have generated past epidemics (e.g., H1N1) could resurge decades after they have apparently disappeared.

    PMID: 21356135 [PubMed - in process]</r0></r0></r0>

  • #2
    Re: Emergence and dynamics of influenza super-strains

    For some reason there is a numeric formatting problem when copying this abstract to FluTrackers.

    Below is a screen shot of the complete abstract.

    Coburn et al.jpg


    • #3
      Re: Emergence and dynamics of influenza super-strains

      This story is recalling the 'recycling' influenza virus theory, I suspect.

      But in the case of H1N1 (2009), are we sure that the virus IS THE SAME that circulated in humans in the early decades of XX century?

      From an antigenic point of view, the answer could be positive, but genetically the two viruses (the spanish-flu-derived H1N1 and current H1N1 2009) cannot be more different.

      So, what is the point?

      Is perhaps the Edwin Kilbourne (recently passed away) theory of 'default' human influenza strains (H1, H2, H3...)?


      • #4
        Re: Emergence and dynamics of influenza super-strains

        A big surprise to many?and a source of terminological confusion?was that the H1N1 virus is not a new subtype. As an H1N1 virus, it is the same subtype as the virus that caused the 1918 pandemic and whose descendants have circulated in humans ever since, except for one 20-year interruption.

        As virologist Vincent Racaniello, PhD, of Columbia University describes it, the H1N1 virus of 1918 went into both people and pigs at the time and evolved on mostly separate tracks in the two different hosts. In humans the subtype circulated until 1957, when it was replaced by the H2N2 virus, which triggered the pandemic of 1957-58. H1N1 then vanished from humans until 1977, when it mysteriously reappeared, probably as the result of a lab accident. It then continued to evolve as one of three seasonal flu strains, with H3N2 and type B.

        Meanwhile, the H1N1 in pigs continued to circulate, but evolved much more slowly than its human counterpart, according to Racaniello, who authors "Virology Blog." Because pigs, as food animals, don't live very long, their viruses don't face very much selection pressure, he explained. "So that virus that went into them in 1918 didn't change very much. It did reaasort with a variety of human and avian viruses, but the key proteins, the HA and NA, are direct descendants and haven't changed very much. To me that's the most amazing thing, that pigs have almost been like a freezer for this virus."

        While the H1N1 in pigs changed little, human strains of H1N1 changed a lot, under pressure from the immune system of their long-lived hosts, Racaniello said. By 2009, the human and pig versions were so different that when the swine version jumped into humans, many people had little protection against it.


        • #5
          their "recombination" is what we usually call reassortment. Our recombination is sometimes
          called "mosaicism"
          I'm interested in expert panflu damage estimates
          my current links: ILI-charts: