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Shiftless, A Critical Piece of the Innate Immune Response to Viral Infection
Version 1
: Received: 6 May 2022 / Approved: 9 May 2022 / Online: 9 May 2022 (05:57:15 CEST)
A peer-reviewed article of this Preprint also exists.
Rodriguez, W.; Muller, M. Shiftless, a Critical Piece of the Innate Immune Response to Viral Infection. Viruses 2022, 14, 1338. Rodriguez, W.; Muller, M. Shiftless, a Critical Piece of the Innate Immune Response to Viral Infection. Viruses 2022, 14, 1338.
Abstract
Since its initial characterization in 2016, the interferon stimulated gene Shiftless (SHFL) has proven to be a critical piece of the innate immune response to viral infection. SHFL expression stringently restricts the replication of multiple DNA, RNA, and retroviruses with an extraordinary diversity of mechanisms that differ from one virus to the next. These inhibitory strategies include the negative regulation of viral RNA stability, translation, and even the manipulation of RNA granule formation during viral infection. Even more surprisingly, SHFL is the first human protein found to directly inhibit the activity of the -1 programmed ribosomal frameshift, a translation recoding strategy utilized across nearly all domains of life and a several human viruses. Recent literature has shown that SHFL expression also significantly impacts viral pathogenesis in mouse models, highlighting its in-vivo efficacy. To help reconcile the many mechanisms by which SHFL restricts viral replication, we provide here a comprehensive review of this complex ISG, its influence over viral RNA fate, and the implications of its functions on the virus-host arms race for control of the cell.
Keywords
C19ORF66; FLJ11286; shiftless; SVA-1; RyDEN; IRAV; ISG; innate immune response; RNA stabil-ity; translation; RNA granules; ribosomal frameshift
Subject
Biology and Life Sciences, Virology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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