Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Nsp4 Cleaves VISA to Impair Antiviral Responses Mediated by RIG-I-like Receptors

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dc.contributor.author Huang, C.
dc.contributor.author Du, Y. P.
dc.contributor.author Yu, Z. B.
dc.contributor.author Zhang, Q.
dc.contributor.author Liu, Y. H.
dc.contributor.author Tang, J.
dc.contributor.author Shi, Jishu
dc.contributor.author Feng, W. H.
dc.date.accessioned 2017-02-14T22:47:52Z
dc.date.available 2017-02-14T22:47:52Z
dc.date.issued 2016-06-22
dc.identifier.uri http://hdl.handle.net/2097/35113
dc.description Citation: Huang, C., Du, Y. P., Yu, Z. B., Zhang, Q., Liu, Y. H., Tang, J., . . . Feng, W. H. (2016). Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Nsp4 Cleaves VISA to Impair Antiviral Responses Mediated by RIG-I-like Receptors. Scientific Reports, 6, 13. https://doi.org/10.1038/srep28497
dc.description.abstract Porcine reproductive and respiratory syndrome virus (PRRSV) is one of the most significant etiological agents in the swine industry worldwide. It has been reported that PRRSV infection can modulate host immune responses, and innate immune evasion is thought to play a vital role in PRRSV pathogenesis. In this study, we demonstrated that highly pathogenic PRRSV (HP-PRRSV) infection specifically down-regulated virus-induced signaling adaptor (VISA), a unique adaptor molecule that is essential for retinoic acid induced gene-I (RIG-I) and melanoma differentiation associated gene 5 (MDA5) signal transduction. Moreover, we verified that nsp4 inhibited IRF3 activation induced by signaling molecules, including RIG-I, MDA5, VISA, and TBK1, but not IRF3. Subsequently, we demonstrated that HP-PRRSV nsp4 down-regulated VISA and suppressed type I IFN induction. Importantly, VISA was cleaved by nsp4 and released from mitochondrial membrane, which interrupted the downstream signaling of VISA. However, catalytically inactive mutant of nsp4 abolished its ability to cleave VISA. Interestingly, nsp4 of typical PRRSV strain CH-1a had no effect on VISA. Taken together, these findings reveal a strategy evolved by HP-PRRSV to counteract anti-viral innate immune signaling, which complements the known PRRSV-mediated immune-evasion mechanisms.
dc.relation.uri https://doi.org/10.1038/srep28497
dc.rights Attribution 4.0 International (CC BY 4.0)
dc.rights.uri https://creativecommons.org/licenses/by/4.0/
dc.subject Pattern-Recognition Receptors
dc.subject Interferon-Stimulated Genes
dc.subject Innate
dc.subject Immune-Responses
dc.subject Nonstructural Protein 4
dc.subject Toll-Like Receptors
dc.title Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Nsp4 Cleaves VISA to Impair Antiviral Responses Mediated by RIG-I-like Receptors
dc.type Article
dc.date.published 2016
dc.citation.doi 10.1038/srep28497
dc.citation.issn 2045-2322
dc.citation.jtitle Scientific Reports
dc.citation.spage 13
dc.citation.volume 6
dc.citation Huang, C., Du, Y. P., Yu, Z. B., Zhang, Q., Liu, Y. H., Tang, J., . . . Feng, W. H. (2016). Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Nsp4 Cleaves VISA to Impair Antiviral Responses Mediated by RIG-I-like Receptors. Scientific Reports, 6, 13. https://doi.org/10.1038/srep28497
dc.contributor.authoreid jshi
dc.contributor.kstate Shi, Jishu


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