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1918 H1N1 influenza virus replicates and induces pro-inflammatory cytokine responses in extra-respiratory tissues of ferrets

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  • 1918 H1N1 influenza virus replicates and induces pro-inflammatory cytokine responses in extra-respiratory tissues of ferrets

    J Infect Dis. 2018 Jan 10. doi: 10.1093/infdis/jiy003. [Epub ahead of print]
    1918 H1N1 influenza virus replicates and induces pro-inflammatory cytokine responses in extra-respiratory tissues of ferrets.

    de Wit E1, Siegers J2, Cronin JM1, Weatherman S1, van den Brand J2, Leijten LM2, van Run P2, Begeman L2, van den Ham HJ2, Andeweg AC2, Bushmaker T1, Scott DP3, Saturday G3, Munster VJ1, Feldmann H1, van Riel D2.
    Author information

    Abstract

    Background:

    The 1918 Spanish H1N1 influenza pandemic was the most severe recorded influenza pandemic with an estimated 20-50 million deaths worldwide. Even though it is known that influenza viruses can cause extra-respiratory tract complications-which are often severe or even fatal- the potential contribution of extra-respiratory tissues to the pathogenesis of 1918 H1N1 virus infection has not been studied comprehensively.
    Methods:

    Here, we performed a time course study in ferrets inoculated intranasally with 1918 H1N1 virus, with special emphasis on the involvement of extra-respiratory tissues. Respiratory and extra-respiratory tissues were collected after inoculation for virological, histological and immunological analysis.
    Results:

    Infectious virus was detected at high titers in respiratory tissues, and-at lower titers-in most extra-respiratory tissues. Evidence for active virus replication, as indicated by the detection of nucleoprotein by immunohistochemistry, was observed in the respiratory tract, peripheral and central nervous system, and liver. Pro-inflammatory cytokines were upregulated in respiratory tissues, olfactory bulb, spinal cord, liver, heart and pancreas.
    Conclusions:

    1918 H1N1 virus spread to, and induced cytokine responses in tissues outside the respiratory tract, which likely contributed to the severity of infection. Moreover, our data support the suggested link between 1918 H1N1 infection and CNS disease.


    KEYWORDS:

    1918 H1N1 virus; CNS disease; animal model; cytokine; extra-respiratory; ferret model; inflamma; influenza A virus; pathogenesis

    PMID: 29329410 DOI: 10.1093/infdis/jiy003
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