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Start Over Author "Ruiqiao Li" Journal frontiers in immunology
2 results on '"Ruiqiao Li"'

1. Dual Regulation of Host TRAIP Post-translation and Nuclear/Plasma Distribution by Porcine Reproductive and Respiratory Syndrome Virus Non-structural Protein 1α Promotes Viral Proliferation

Author

Peidian Shi, Yanxin Su, Ruiqiao Li, Lei Zhang, Chen Chen, Lilin Zhang, Kay Faaberg, and Jinhai Huang

Subjects
PRRSV, TRAIP, nsp1α, SUMOylation, IFN, TBK1, Immunologic diseases. Allergy, RC581-607
Abstract

In this study, we show that porcine reproductive and respiratory syndrome virus (PRRSV) non-structural protein 1α (nsp1α) facilitates PRRSV escape from innate immune by modulating nuclear to cytoplasmic translocation and distribution ratio of TRAIP to promote virus proliferation. Mechanistically, TRAIP interacts with PRRSV nsp1α via its K205 site, while NSP1α decreases the SUMOylation and K48 ubiquitination independent of the TRAIP interaction K205 site. Modulation of the dual modification of TRAIP by PRRSV nsp1α results in over-enrichment of TRAIP in the cytoplasm. Enrichment of nsp1α-induced cytoplasmic TRAIP in turn leads to excessive K48 ubiquitination and degradation of serine/threonine-protein kinase (TBK1), thereby antagonizing TBK1-IRF3-IFN signaling. This study proposes a novel mechanism by which PRRSV utilizes host proteins to regulate innate immunity. Findings from this study provides novel perspective to advance our understanding in the pathogenesis of PRRSV.

Published
2018
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2. Dual Regulation of Host TRAIP Post-translation and Nuclear/Plasma Distribution by Porcine Reproductive and Respiratory Syndrome Virus Non-structural Protein 1α Promotes Viral Proliferation

Author

Chen Chen, Lilin Zhang, Kay S. Faaberg, Jinhai Huang, Yanxin Su, Ruiqiao Li, Peidian Shi, and Lei Zhang

Subjects
0301 basic medicine, Cytoplasm, Swine, TBK1, viruses, animal diseases, Sus scrofa, SUMO protein, Viral Nonstructural Proteins, Virus Replication, Mice, Ubiquitin, TANK-binding kinase 1, Immunology and Allergy, RNA, Small Interfering, Original Research, Mice, Inbred BALB C, Kinase, virus diseases, Translation (biology), SUMOylation, Cell biology, TRAIP, Host-Pathogen Interactions, Interferon Type I, lcsh:Immunologic diseases. Allergy, Ubiquitin-Protein Ligases, Immunology, Porcine Reproductive and Respiratory Syndrome, Biology, IFN, Virus, 03 medical and health sciences, Animals, Humans, Porcine respiratory and reproductive syndrome virus, Cell Nucleus, Innate immune system, 030102 biochemistry & molecular biology, Ubiquitination, Porcine reproductive and respiratory syndrome virus, biology.organism_classification, Immunity, Innate, nsp1α, HEK293 Cells, 030104 developmental biology, PRRSV, biology.protein, lcsh:RC581-607, HeLa Cells
Abstract

In this study, we show that porcine reproductive and respiratory syndrome virus (PRRSV) non-structural protein 1α (nsp1α) facilitates PRRSV escape from innate immune by modulating nuclear to cytoplasmic translocation and distribution ratio of TRAIP to promote virus proliferation. Mechanistically, TRAIP interacts with PRRSV nsp1α via its K205 site, while NSP1α decreases the SUMOylation and K48 ubiquitination independent of the TRAIP interaction K205 site. Modulation of the dual modification of TRAIP by PRRSV nsp1α results in over-enrichment of TRAIP in the cytoplasm. Enrichment of nsp1α-induced cytoplasmic TRAIP in turn leads to excessive K48 ubiquitination and degradation of serine/threonine-protein kinase (TBK1), thereby antagonizing TBK1-IRF3-IFN signaling. This study proposes a novel mechanism by which PRRSV utilizes host proteins to regulate innate immunity. Findings from this study provides novel perspective to advance our understanding in the pathogenesis of PRRSV.

Published
2018
Full Text
View/download PDF

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