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The present study was undertaken to clarify the role of Sendai virus (SeV) V protein, which has been shown to downregulate IFN-β induction through inhibition of IRF-3 activation, in viral pathogenesis. Mice infected with rSeV mutants, deficient in V expression or expressing V lacking the C-terminus, had several-fold higher IFN activity levels in the lungs than those in wild-type virus-infected mice,...
Sendai virus C protein (SeV C) has been reported to counteract the antiviral activities of interferons (IFNs) by inhibiting the expression of IFN-stimulated gene products. In SeV C-expressing cells, formation of an active ISGF3 complex and translocation of STAT1 into the nucleus were not observed. STAT1 was continuously phosphorylated at tyrosine 701 by IFN signaling; however, its serine phosphorylation...
Sendai virus (SeV) renders cells unresponsive to interferon (IFN)-α. To identify viral factors involved in this process, we examined whether recombinant SeVs, which could not express V protein, subsets of C proteins (C, C', Y1 and Y2) or any of four C proteins, retained the capability of impeding IFN-α-mediated responses. Among these viruses, only the 4C knockout virus completely lost the ability...
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