Vesicular stomatitis virus infection induces a nuclear DNA-binding factor specific for the interferon-stimulated response element.

摘要: Vesicular stomatitis virus (VSV) has a broad host range. It replicates in the cytoplasm and causes rapid cytopathic effects. We show that following VSV infection, nuclear factor binds to select set of interferon-stimulated responsive elements (ISRE) is induced many cell types. This factor, tentatively called VSV-induced binding protein (VIBP), was estimated have an approximate molecular mass 50 kDa distinct from known members interferon regulatory family, are bind ISRE. Induction VIBP required tyrosine kinase activity but did not require cellular transcription. Treatment cells with cycloheximide, which inhibits translation, only partially inhibited induction VIBP. However, type I interferons staurosporine, both inhibit transcription, induction. Moreover, double-stranded RNA analog, poly(I)-poly(C) also DNA-binding very similar These results indicate preexisting activated upon infection this activation requires primary viral transcripts. The functional analyzed stably transfected herpesvirus thymidine kinase-luciferase reporter gene under control While promoter without ISRE strongly (as result virus-mediated transcriptional shutdown cell), inhibition reversed by ISRE-containing promoter, albeit partially, suggests differentially affects transcription genes. Although all other tested, it embryonal carcinoma after suggesting developmental regulation inducibility.