Changing Epstein-Barr viral ZEBRA protein into a more powerful activator enhances its capacity to disrupt latency.
AUTOR(ES)
Baumann, R
RESUMO
The Epstein-Barr viral transcriptional activator ZEBRA induces expression of viral early lytic genes when introduced into cells bearing latent Epstein-Barr virus. We show here that a ZEBRA-herpes simplex viral protein 16 (VP16) fusion protein induces early viral lytic gene expression in Epstein-Barr virus-containing cells more efficiently than does wild-type ZEBRA. The fusion protein is also a more powerful transcriptional activator in these cells, as assayed with reporter constructs. Our experiments also suggest that ZEBRA manifests a function required for full activity on certain natural promoters but not on promoters bearing oligomerized ZEBRA binding sites; this function cannot be provided by VP16.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=46526Documentos Relacionados
- Epstein-Barr virus with heterogeneous DNA disrupts latency.
- Polymorphic proteins encoded within BZLF1 of defective and standard Epstein-Barr viruses disrupt latency.
- Alteration of a single serine in the basic domain of the Epstein-Barr virus ZEBRA protein separates its functions of transcriptional activation and disruption of latency.
- Eradication of Epstein-Barr virus by allogeneic bone marrow transplantation: implications for sites of viral latency.
- IRF-7, a new interferon regulatory factor associated with Epstein-Barr virus latency.
