title: Severe fever with thrombocytopenia syndrome virus inhibits exogenous Type I IFN signaling pathway through its NSs invitro.
abstract: Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus (SFTS virus, SFTSV). At present there is still no specific antiviral treatment for SFTSV; To understand which cells support SFTSV life cycle and whether SFTSV infection activates host innate immunity, four different cell lines (Vero, Hela, Huh7.5.1, and Huh7.0) were infected with SFTSV. Intracellular/extracellular viral RNA and expression of IFNα, and IFNß were detected by real-time RT- PCR following infection. To confirm the role of non-structural protein (NSs) of SFTSV in exogenous IFNα-induced Jak/STAT signaling, p-STAT1 (Western Blot), ISRE activity (Luciferase assay) and ISG expression (real-time PCR) were examined following IFNα stimulation in the presence or absence of over-expression of NSs in Hela cells. Our study showed that all the four cell lines supported SFTSV life cycle and SFTSV activated host innate immunity to produce type I IFNs in Hela cells but not in Huh7.0, Huh7.5.1 or Vero cells. NSs inhibited exogenous IFNα-induced Jak/STAT signaling as shown by decreased p-STAT1 level, suppressed ISRE activity and down-regulated ISG expression. Suppression of the exogenous Type I IFN-induced Jak/STAT signaling by NSs might be one of the mechanisms of SFTSV to evade host immune surveillance.
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Chen
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Ye
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
authors.forename: Shilin
authors.initials: S
authors.lastname: Li
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
authors.forename: Baihai
authors.initials: B
authors.lastname: Jiao
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.
authors.forename: Jianqin
authors.initials: J
authors.lastname: Wu
authors.affiliation: West China School of Public Health, Sichuan University, Chengdu, Sichuan, China.
authors.forename: Peibin
authors.initials: P
authors.lastname: Zeng
authors.affiliation: Institute of Blood Transfusion, Chinese Academic of Medical Sciences and Peking Union Medical College, Chengdu, China.|Toronto General Research Institute, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Limin
authors.initials: L
authors.lastname: Chen
mesh_terms: D000818:Animals; D002044:Bunyaviridae Infections / Q000235:genetics* / Q000821:virology; D002522:Chlorocebus aethiops; D006367:HeLa Cells; D006790:Host-Parasite Interactions / Q000235:genetics; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D007370:Interferon Type I / Q000037:antagonists & inhibitors / Q000235:genetics*; D016856:Phlebovirus / Q000235:genetics* / Q000472:pathogenicity; D015398:Signal Transduction / Q000235:genetics; D014709:Vero Cells; D017361:Viral Nonstructural Proteins / Q000235:genetics*
chemical_list: D007370:Interferon Type I; D017361:Viral Nonstructural Proteins