Home Acta Virologica 2017 Acta Virologica Vol.61, No.3, p.289-298, 2017

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Founded: 1957
ISSN 0001-723X
E-ISSN 1336-2305

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Acta Virologica Vol.61, No.3, p.289-298, 2017

Title: NSs protein of severe fever with thrombocytopenia syndrome virus suppresses interferon production through different mechanism than Rift Valley fever virus
Author: S. ZHANG, B. ZHENG, T. WANG, A. LI, J. WAN, J. QU, CH. LI, D. LI, M. LIANG

Abstract: Severe fever with thrombocytopenia syndrome virus (SFTSV) is a newly identified Phlebovirus that causes severe fever with thrombocytopenia syndrome. Our study demonstrated that SFTSV NSs functioned as IFN antagonist mainly by suppressing TBK1/IKKε−IRF3 signaling pathway. NSs interacted with and relocalized TANK-binding kinase 1 (TBK1) into NSs-induced cytoplasmic structures and this interaction could effectively inhibit downstream phosphorylation and dimerization of interferon regulatory factor 3 (IRF3), resulting in the suppression of antiviral signaling and IFN induction. Functional sites of SFTSV NSs binding with TBK1 were then studied and results showed that NSs had lost their IFN-inhibiting activity after deleting the 25 amino acids in N-terminal. Furthermore, the mechanism of Rift Valley fever virus (RVFV) NSs blocking IFN-β response were also investigated. Preliminary results showed that RVFV NSs proteins could neither interact nor co-localize with TBK1 in cytoplasm, but suppressed its expression levels, phosphorylation and dimerization of IRF3 in the subsequent steps, resulting in inhibition of the IFN-β production. Altogether, our data demonstrated the probable mechanism used by SFTSV to inhibit IFN responses which was different from RVFV and pointed toward a novel mechanism for RVFV suppressing IFN responses.

Keywords: SFTS virus; NSs protein; interferon signaling; TBK1/IKKε–IRF3
Published online: 28-Aug-2017
Year: 2017, Volume: 61, Issue: 3 Page From: 289, Page To: 298
doi:10.4149/av_2017_307


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