Trans-Repression of protein expression dependent on the Epstein-Barr virus promoter Wp during latency.

ABSTRACT: An ordered silencing of Epstein-Barr virus (EBV) latency gene transcription is critical for establishment of persistent infection within B lymphocytes, yet the mechanisms responsible and the role that the virus itself may play are unclear. Here we describe two B-cell superinfection models with which to address these problems. In the first, Burkitt lymphoma (BL) cells that maintain latency I, when superinfected, initially supported transcription from the common EBNA promoters Wp and Cp (latency III) but ultimately transitioned to latency I (Cp/Wp silent), an essential requirement for establishment of EBV latency in vivo. We used this model to test whether the early lytic-cycle gene BHLF1, implicated in silencing of the Cp/Wp locus, is required to establish latency I. Upon superinfection wit

SUBMITTER: Hughes DJ 

PROVIDER: S-EPMC3194970 | biostudies-literature | 2011 Nov

REPOSITORIES: biostudies-literature