CHANGING EPSTEIN-BARR VIRAL ZEBRA PROTEIN INTO A MORE POWERFUL ACTIVATOR ENHANCES ITS CAPACITY TO DISRUPT LATENCY

The Epstein-Barr viral transcriptional activator ZEBRA induces express ion of viral early lytic genes when introduced into cells bearing late nt Epstein-Barr virus. We show here that a ZEBRA-herpes simplex viral protein 16 (VP16) fusion protein induces early viral lytic gene expres sion in Epstein-Barr virus-containing cells more efficiently than does wild-type ZEBRA. The fusion protein is also a more powerful transcrip tional 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 be aring oligomerized ZEBRA binding sites; this function cannot be provid ed by VP16.