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.
Highlights
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus (SFTSV) firstly identified in China with initial mortality rates ranging from 6.3% to 30%[1,2,3]
Human liver cancer cell lines Huh7.0 (TLR3 -/-) and Huh7.5.1 (TLR-/- retinoic acid-inducible gene protein (RIG-I) -/-) were infected with SFTSV (MOI = 1.0) for 2 hours and cultured for 48hours, expression RNA levels of IFNα and IFNβ were quantified by real-time PCR
The protein levels of IFNα and IFNβ in culture medium of Human cervical cancer cell line (Hela) cells and Vero cells were determined by ELISA, and we found that IFNα and IFNβ were up-regulated in the culture medium of Hela cells but not in Vero cells stimulated by SFTSV as shown in Fig 2D, These results collectively demonstrated that SFTSV may activate host innate immunity through TLR3 signaling pathway
Summary
Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel bunyavirus (SFTSV) firstly identified in China with initial mortality rates ranging from 6.3% to 30%[1,2,3]. Clinical manifestation of SFTSV infection includes severe fever, thrombocytopenia and leukocytopenia, and the disease process consists of four stages: incubation, severe fever, multiple organ failure, and convalescence[4, 5]. As a tick-borne disease, SFTS mainly occurred between April and October, and peaked in May to July[6]. Most of patients were farmers in endemic areas due to high risk of exposures to tick-biting[6].
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