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National Academy of Sciences, Proceedings of the National Academy of Sciences, 42(103), p. 15535-15539, 2006

DOI: 10.1073/pnas.0607325103

Elsevier, Year Book of Pathology and Laboratory Medicine, (2008), p. 344-345

DOI: 10.1016/s1077-9108(08)70748-5

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Increased susceptibility to bacterial superinfection as a consequence of innate antiviral responses

Journal article published in 2006 by Alexander A. Navarini, Navarini Aa, Mike Recher, Karl S. Lang, Lang Ks, Panco Georgiev, Susanne Meury, Andreas Bergthaler ORCID, Lukas Flatz, Jacques Bille, Regine Landmann, Bernhard Odermatt, Hans Hengartner, M. G. Bissell, Rolf M. Zinkernagel and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

The reason why severe localized or systemic virus infections enhance and aggravate bacterial superinfection is poorly understood. Here we show that virus-induced IFN type I caused apoptosis in bone marrow granulocytes, drastically reduced granulocyte infiltrates at the site of bacterial superinfection, caused up to 1,000-fold higher bacterial titers in solid organs, and increased disease susceptibility. The finding that the innate antiviral immune response reduces the antibacterial granulocyte defense offers an explanation for enhanced susceptibility to bacterial superinfection during viral disease.