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Cell Rep. 2014 Jul 10;8(1):114-25. doi: 10.1016/j.celrep.2014.05.038. Epub 2014 Jun 19.

The Mammalian response to virus infection is independent of small RNA silencing.

Author information

1
Department of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
2
Department of Genetics and Genomic Sciences, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA.
3
Department of Microbiology, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Global Health and Emerging Pathogens Institute, Icahn Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA. Electronic address: benjamin.tenoever@mssm.edu.

Abstract

A successful cellular response to virus infection is essential for evolutionary survival. In plants, arthropods, and nematodes, cellular antiviral defenses rely on RNAi. Interestingly, the mammalian response to virus is predominantly orchestrated through interferon (IFN)-mediated induction of antiviral proteins. Despite the potency of the IFN system, it remains unclear whether mammals also have the capacity to employ antiviral RNAi. Here, we investigated this by disabling IFN function, small RNA function, or both activities in the context of virus infection. We find that loss of small RNAs in the context of an in vivo RNA virus infection lowers titers due to reduced transcriptional repression of the host antiviral response. In contrast, enabling a virus with the capacity to inhibit the IFN system results in increased titers. Taken together, these results indicate that small RNA silencing is not a physiological contributor to the IFN-mediated cellular response to virus infection.

PMID:
24953656
PMCID:
PMC4096324
DOI:
10.1016/j.celrep.2014.05.038
[Indexed for MEDLINE]
Free PMC Article
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