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Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis

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  • Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis

    Virology. 2018 Oct 31;526:155-164. doi: 10.1016/j.virol.2018.10.017. [Epub ahead of print]
    Lack of IFNγ signaling attenuates spread of influenza A virus in vivo and leads to reduced pathogenesis.

    Nicol MQ1, Campbell GM1, Shaw DJ1, Dransfield I2, Ligertwood Y1, Beard PM3, Nash AA1, Dutia BM4.
    Author information

    Abstract

    IFNγ is a key regulator of inflammatory responses but its role in influenza A virus (IAV) pathogenesis is unclear. Our studies show that infection of mice lacking the IFNγ receptor (IFNγR-/-) at a dose which caused severe disease in wild type 129 Sv/Ev (WT) mice resulted in milder clinical symptoms and significantly lower lung virus titers by 6 days post-infection (dpi). Viral spread was reduced in IFNγR-/- lungs at 2 and 4 dpi. Levels of inflammatory cytokines and chemokines were lower in IFNγR-/- mice at 2 dpi and there was less infiltration of monocyte/macrophage lineage cells than in WT mice. There was no difference in CD4+ and CD8+ T cells and alveolar macrophages in the bronchoalveolar lavage fluid (BALF) at 2 and 4 dpi but by 4 dpi IFNγR-/- mice had significantly higher percentages of neutrophils. Our data strongly suggest that IAV can use the inflammatory response to promote viral spread.


    KEYWORDS:

    Host response; IFNγ; Influenza A virus; Lung inflammation

    PMID: 30390564 DOI: 10.1016/j.virol.2018.10.017
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