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Nonstructural Protein of Severe Fever with Thrombocytopenia Syndrome Phlebovirus Inhibits TBK1 to Evade Interferon-Mediated Response

Authors
Lee, Jae KyungShin, Ok Sarah
Issue Date
2월-2021
Publisher
KOREAN SOC MICROBIOLOGY & BIOTECHNOLOGY
Keywords
SFTSV NSs; inclusion bodies; TBK1; innate immune response
Citation
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY, v.31, no.2, pp.226 - 232
Indexed
SCIE
SCOPUS
KCI
Journal Title
JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
Volume
31
Number
2
Start Page
226
End Page
232
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/49640
DOI
10.4014/jmb.2008.08048
ISSN
1017-7825
Abstract
Severe fever with thrombocytopenia syndrome virus (SFTSV) is an emerging phlebovirus of the Phenuiviridae family that has been circulating in the following Asian countries: Vietnam, Myanmar, Taiwan, China, Japan, and South Korea. Despite the increasing infection rates and relatively high mortality rate, there is limited information available regarding SFTSV pathogenesis. In addition, there are currently no vaccines or effective antiviral treatments available. Previous reports have shown that SFTSV suppresses the host immune response and its nonstructural proteins (NSs) function as an antagonist of type I interferon (IFN), whose induction is an essential part of the host defense system against viral infections. Given that SFTSV NSs suppress the innate immune response by inhibiting type I IFN, we investigated the mechanism utilized by SFTSV NSs to evade IFNmediated response. Our co-immunoprecipitation data suggest the interactions between NSs and retinoic acid inducible gene-I (RIG-I) or TANK binding kinase 1 (TBK1). Furthermore, confocal analysis indicates the ability of NSs to sequester RIG-I and related downstream molecules in the cytoplasmic structures called inclusion bodies (IBs). NSs are also capable of inhibiting TBK1interferon regulatory factor 3 (IRF3) interaction, and therefore prevent the phosphorylation and nuclear translocation of IRF3 for the induction of type I IFN. The ability of SFTSV NSs to interact with and sequester TBK1 and IRF3 in IBs demonstrate an effective yet unique method utilized by SFTSV to evade and suppress host immunity.
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