Rotavirus NSP1 Inhibits Type I and Type III Interferon Induction

Iaconis, Gennaro, Jackson, Ben, Childs, Kay, Boyce, Mark, Goodbourn, Stephen, Blake, Neil, Iturriza-Gomara, Miren ORCID: 0000-0001-5816-6423 and Seago, Julian (2021) Rotavirus NSP1 Inhibits Type I and Type III Interferon Induction. VIRUSES-BASEL, 13 (4). 589-.

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Official URL: http://dx.doi.org/10.3390/v13040589

Abstract

Type I interferons (IFNs) are produced by most cells in response to virus infection and stimulate a program of anti-viral gene expression in neighboring cells to suppress virus replication. Type III IFNs have similar properties, however their effects are limited to epithelial cells at mucosal surfaces due to restricted expression of the type III IFN receptor. Rotavirus (RV) replicates in intestinal epithelial cells that respond predominantly to type III IFNs, and it has been shown that type III rather than type I IFNs are important for controlling RV infections in vivo. The RV NSP1 protein antagonizes the host type I IFN response by targeting IRF-3, IRF-5, IRF-7, or β-TrCP for proteasome-mediated degradation in a strain-specific manner. Here we provide the first demonstration that NSP1 proteins from several human and animal RV strains antagonize type III as well as type I IFN induction. We also show that NSP1 is a potent inhibitor of IRF-1, a previously undescribed property of NSP1 which is conserved among human and animal RVs. Interestingly, all NSP1 proteins were substantially more effective inhibitors of IRF-1 than either IRF-3 or IRF-7 which has significance for evasion of basal anti-viral immunity and type III IFN induction in the intestinal epithelium.

Item Type:	Article
Uncontrolled Keywords:	rotavirus, type I interferon, type III interferon, NSP1, IRF-1, IRF-3, IRF-7, NF-&#954, B
Divisions:	Faculty of Health and Life Sciences Faculty of Health and Life Sciences > Institute of Infection, Veterinary and Ecological Sciences
Depositing User:	Symplectic Admin
Date Deposited:	12 May 2021 09:57
Last Modified:	18 Jan 2023 22:47
DOI:	10.3390/v13040589
Open Access URL:	https://doi.org/10.3390/v13040589
Related URLs:	Author Publisher
URI:	https://livrepository.liverpool.ac.uk/id/eprint/3122444