Interferon-independent and -induced regulation of Epstein-Barr virus EBNA-1 gene transcription in Burkitt lymphoma.

摘要: Replication of the Epstein-Barr virus (EBV) genome within latently infected cells is dependent on EBV EBNA-1 protein. The objective this study was to identify transcriptional regulatory proteins that mediate expression via viral promoter Qp, which active in EBV-associated tumors such as Burkitt lymphoma and nasopharyngeal carcinoma. Results a yeast one-hybrid screen suggested subset interferon factor (IRF) family may regulate transcription by targeting an essential cis-regulatory element QRE-2. Further investigation indicated activator IRF-1 closely related IRF-2, repressor interferon-induced gene expression, are both capable activating Qp. However, major QRE-2-specific binding activity detected extracts attributed suggesting interferon-independent activation Qp largely mediated IRF-2 these cells. We observed no effect gamma transfection assays, whereas we moderate but significant repression response alpha interferon, possibly either consensus sequence protein or IRF-7, novel interferon-inducible identified study. Since increased interferons, presence likely represented equilibrium between IRF factors activate those repress interferon. Thus, usurping its antagonist has evolved not only mechanism constitutively express also one sustain face antiviral effects