ArticleJournal of virology2011
Diversity of interferon antagonist activities mediated by NSP1 proteins of different rotavirus strains.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
54 citing papers in PubMed, 91 citations in OpenAlex.
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- Re-Examining Rotavirus Innate Immune Evasion: Potential Applications of the Reverse Genetics System.mBio · 2022Review
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- Viral pathogen-induced mechanisms to antagonize mammalian interferon (IFN) signaling pathway.Cellular and molecular life sciences : CMLS · 2021Review
- Rotavirus Interactions With Host Intestinal Epithelial Cells.Frontiers in immunology · 2021Review
- Rotavirus Reprograms Multiple Interferon Receptors and Restricts Their Intestinal Antiviral and Inflammatory Functions.Journal of virology · 2020Article
- Reverse Genetics System for a Human Group A Rotavirus.Journal of virology · 2020Article
- Intragenic recombination influences rotavirus diversity and evolution.Virus evolution · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Studies involving limited numbers of rotavirus (RV) strains have shown that the viral gene 5 product, NSP1, can antagonize beta interferon (IFN-β) expression by inducing the degradation of IFN-regulatory factors (IRFs) (IRF3, IRF5, and IRF7) or a component of the E3 ubiquitin ligase complex responsible for activating NF-κB (β-transducin repeat-containing protein [β-TrCP]). To gain a broader perspective of NSP1 activities, we examined various RV strains for the ability to inhibit IFN-β expression in human cells. We found that all strains encoding wild-type NSP1 impeded IFN-β expression but not always through IRF3 degradation. To identify other degradation targets involved in suppressing IFN-β expression, we used transient expression vectors to test the abilities of a diverse collection of NSP1 proteins to target IRF3, IRF5, IRF7, and β-TrCP for degradation. The results indicated that human RVs rely predominantly on the NSP1-induced degradation of IRF5 and IRF7 to suppress IFN signaling, whereas NSP1 proteins of animal RVs tended to target IRF3, IRF5, and IRF7, allowing the animal viruses a broader attack on the IFN-β signaling pathway. The results also suggested that the NSP1-induced degradation of β-TrCP is an uncommon mechanism of subverting IFN-β signaling but is one that can be shared with NSP1 proteins that induce IRF degradation. Our analysis reveals that the activities of NSP1 proteins are diverse, with no obvious correlations between degradations of pairs of target proteins. Thus, RVs have evolved functionally distinct approaches for subverting the host antiviral response, a property consistent with the immense sequence variation noted for NSP1 proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.