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    Influenza A Viruses Target Type II Pneumocytes in the Human Lung (2012)

    Art
    Zeitschriftenartikel / wissenschaftlicher Beitrag
    Autoren
    Weinheimer, Viola K
    Becher, Anne
    Tönnies, Mario
    Holland, Gudrun
    Knepper, Jessica
    Bauer, Torsten T
    Schneider, Paul
    Neudecker, Jens
    Rückert, Jens C
    Szymanski, Kolja
    Temmesfeld-Wollbrueck, Bettina
    Gruber, Achim D
    Bannert, Norbert
    Suttorp, Norbert
    Hippenstiel, Stefan
    Wolff, Thorsten
    Hocke, Andreas C
    Quelle
    The Journal of infectious diseases; 206(11) — S. 1685–1694
    ISSN: 0022-1899
    Sprache
    Englisch
    Verweise
    DOI: 10.1093/infdis/jis455
    Pubmed: 22829640
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    Abstract / Zusammenfassung

    Highly pathogenic avian H5N1 influenza viruses preferentially infect alveolar type II pneumocytes in human lung. However, it is unknown whether this cellular tropism contributes to high viral virulence because the primary target cells of other influenza viruses have not been systematically studied.

    We provide the first comparison of the replication, tropism, and cytokine induction of human, highly pathogenic avian influenza A virus subtype H5N1 and other animal influenza A viruses in primary human lung organ cultures.

    Subytpe H5N1 and human-adapted subtype H1N1 and H3N2 viruses replicated efficiently in the lung tissue, whereas classic swine and low-pathogenicity avian viruses propagated only poorly. Nevertheless, all viruses examined were detected almost exclusively in type II pneumocytes, with a minor involvement of alveolar macrophages. Infection with avian viruses that have a low and high pathogenicity provoked a pronounced induction of cytokines and chemokines, while human and pandemic H1N1-2009 viruses triggered only weak responses.

    These findings show that differences in the pathogenic potential of influenza A viruses in the human lung cannot be attributed to a distinct cellular tropism. Rather, high or low viral pathogenicity is associated with a strain-specific capacity to productively replicate in type II pneumocytes and to cope with the induced cytokine response.