作者: S. Saito , T. Murata , T. Kanda , H. Isomura , Y. Narita
DOI: 10.1128/JVI.02020-12
关键词:
摘要: Epstein-Barr virus (EBV), a human oncogenic herpesvirus that establishes lifelong latent infection in the host, occasionally enters lytic to produce progeny viruses. The EBV oncogene membrane protein 1 (LMP1), which is expressed both and infection, constitutively activates canonical NF-κB (p65) pathway. Such LMP1-mediated activation necessary for proliferation of latently infected cells inhibition viral cycle progression. Actually, target gene expression was suppressed upon onset infection. TRAF6, activated by conjugation polyubiquitin chains, associates with LMP1 mediate signal transduction. We have found EBV-encoded BPLF1 interacts deubiquitinates TRAF6 inhibit signaling during HEK293 BPLF1-deficient recombinant exhibited poor DNA replication compared wild type. Furthermore, exogenous or p65 knockdown restored viruses, indicating transduction, leading promotion replication.