Distinct antiviral signatures revealed by the magnitude and round of influenza virus replication in vivo.

Autor:	Sjaastad LE; Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455.; Center for Immunology, University of Minnesota, Minneapolis, MN 55455., Fay EJ; Center for Immunology, University of Minnesota, Minneapolis, MN 55455.; Biochemistry, Molecular Biology and Biophysics Graduate Program, University of Minnesota, Minneapolis, MN 55455., Fiege JK; Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455.; Center for Immunology, University of Minnesota, Minneapolis, MN 55455., Macchietto MG; Institute for Health Informatics, University of Minnesota, Minneapolis, MN 55455., Stone IA; Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455.; Center for Immunology, University of Minnesota, Minneapolis, MN 55455., Markman MW; Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455.; Center for Immunology, University of Minnesota, Minneapolis, MN 55455., Shen S; Institute for Health Informatics, University of Minnesota, Minneapolis, MN 55455., Langlois RA; Department of Microbiology and Immunology, University of Minnesota, Minneapolis, MN 55455; langlois@umn.edu.; Center for Immunology, University of Minnesota, Minneapolis, MN 55455.; Biochemistry, Molecular Biology and Biophysics Graduate Program, University of Minnesota, Minneapolis, MN 55455.
Jazyk:	angličtina
Zdroj:	Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2018 Sep 18; Vol. 115 (38), pp. 9610-9615. Date of Electronic Publication: 2018 Sep 04.
DOI:	10.1073/pnas.1807516115
Abstrakt:	Influenza virus has a broad cellular tropism in the respiratory tract. Infected epithelial cells sense the infection and initiate an antiviral response. To define the antiviral response at the earliest stages of infection we used a series of single-cycle reporter viruses. These viral probes demonstrated cells in vivo harbor a range in magnitude of virus replication. Transcriptional profiling of cells supporting different levels of replication revealed tiers of IFN-stimulated gene expression. Uninfected cells and cells with blunted replication expressed a distinct and potentially protective antiviral signature, while cells with high replication expressed a unique reserve set of antiviral genes. Finally, we used these single-cycle reporter viruses to determine the antiviral landscape during virus spread, which unveiled disparate protection of epithelial cell subsets mediated by IFN in vivo. Together these results highlight the complexity of virus-host interactions within the infected lung and suggest that magnitude and round of replication tune the antiviral response. Competing Interests: The authors declare no conflict of interest.
Databáze:	MEDLINE
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