| Literature DB >> 29186718 |
Keaton M Crosse1, Ebony A Monson, Michael R Beard, Karla J Helbig.
Abstract
The ability of a host to curb a viral infection is heavily reliant on the effectiveness of an initial antiviral innate immune response, resulting in the upregulation of interferon (IFN) and, subsequently, IFN-stimulated genes (ISGs). ISGs serve to mount an antiviral state within a host cell, and although the specific antiviral function of a number of ISGs has been characterized, the function of many of these ISGs remains to be determined. Recent research has uncovered a novel role for a handful of ISGs, some of them directly induced by IFN regulatory factor 3 in the absence of IFN itself. These ISGs, most with potent antiviral activity, are also able to augment varying arms of the innate immune response to viral infection, thereby strengthening this response. This new understanding of the role of ISGs may, in turn, help the recent advancement of novel therapeutics aiming to augment innate signaling pathways in an attempt to control viral infection and pathogenesis.Entities:
Keywords: Innate immunity; Interferon; Interferon-stimulated genes; Virus
Mesh:
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Year: 2017 PMID: 29186718 PMCID: PMC5969054 DOI: 10.1159/000484258
Source DB: PubMed Journal: J Innate Immun ISSN: 1662-811X Impact factor: 7.349