K13 blocks KSHV lytic replication and deregulates vIL6 and hIL6 expression: a model of lytic replication induced clonal selection in viral oncogenesis.

ABSTRACT:

Background

Accumulating evidence suggests that dysregulated expression of lytic genes plays an important role in KSHV (Kaposi's sarcoma associated herpesvirus) tumorigenesis. However, the molecular events leading to the dysregulation of KSHV lytic gene expression program are incompletely understood.

Methodology/principal findings

We have studied the effect of KSHV-encoded latent protein vFLIP K13, a potent activator of the NF-kappaB pathway, on lytic reactivation of the virus. We demonstrate that K13 antagonizes RTA, the KSHV lytic-regulator, and effectively blocks the expression of lytic proteins, production of infectious virions and death of the infected cells. Induction of lytic replication selects for clones with increased K13 expression and NF-kappaB activity, while siR

SUBMITTER: Zhao J 

PROVIDER: S-EPMC2020437 | biostudies-literature | 2007 Oct

REPOSITORIES: biostudies-literature