Search

Group H Rotavirus (RVH) is associated with human diarrhea gastroenteritis. The interferon (IFN) response induced by RVH remains unclear. In this study, we first studied the characteristic feature of RVH and found J19 strain of RVH grew less efficiently compared with the G6P1 strain of RVA. Next, we found that infection with the J19 virus resulted in the secretion of IFN-λ1, but not IFN-β, while both IFN-β and IFN-λ1 could inhibit J19 replication significantly in Caco-2 cells. NSP1 played an important role in the suppression of type I and type III IFN response, and NSP5 protein significantly inhibited activation of IFN-λ1. J19 NSP1 suppressed the induction of IFN-β obviously than G6P1 NSP1, while G6P1 NSP1 reduced IFN-λ1 induction to the greatest extent compared with G9P8, Wa, and J19 NSP1s. Our studies reveal the propagation feature of RVH and interferon induction and suppression by group H rotavirus. • J19 strain of RVH grew less efficiently compared with G6P1 strain of RVA. • J19 Infection resulted in the secretion of IFN-λ1, but not IFN-β. • NSP1 played important role in the suppression of type I and type III IFN response. • J19 NSP1 suppressed the induction of IFN-β obviously than G6P1 NSP1. [ABSTRACT FROM AUTHOR]

Influenza A virus infection activates various intracellular signaling pathways, which is mediated by the transcription factors. Here, a quantitative phosphoproteomic analysis of A549 cells after infection with influenza A virus (H5N1) was performed and we found that the transcription factor STAT1 was highly activated. Unexpectedly, upon inhibition of p-STAT1, titers of progeny virus and viral protein synthesis were both reduced. The STAT1 inhibitor Fludarabine (FLUD) inhibited an early progeny step in viral infection and reduced the levels of influenza virus genomic RNA (vRNA). Concomitantly, there was reduced expression of inflammatory cytokines in p-STAT1 inhibited cells. In vivo , suppression of p-STAT1 improved the survival of H5N1 virus-infected mice, reduced the pulmonary inflammatory response and viral burden. Thus, our data demonstrated a critical role for p-STAT1 in influenza virus replication and inflammatory responses. We speculate that STAT1 is an example of a putative antiviral signaling component to support effective replication. • STAT1 was highly activated after the influenza A virus (IAV) infection. • STAT1 activation was critically involved in vRNA synthesis. • STAT1 phosphorylation could globally affect cytokine expression. • Suppression of STAT1 could improve overall survival of the H5N1-infected animals. [ABSTRACT FROM AUTHOR]