Topological Effects of EBNA 1 on oriP
Abstract
Two processes are required in order to maintain a herpesvirus in a latent state: there must be a mechanism for the viral genome to persist in the cell, and there must be mechanisms to inhibit the expression of those replicative functions which would ordinarily lead to cell death. In the specific case of the Epstein-Barr herpesvirus (EBV), the genome is maintained by an interaction between EBNA 1 and a region of EBV DNA called oriP (1–3). This interaction permits the viral genome to remain extrachromosomal and to partition in concert with cell division. The switch from latency to expression of viral replicative functions is brought about by the ZEBRA gene product (4–7). In latency there must exist a mechanism for inhibiting ZEBRA expression, probably at the transcriptional level (8).
Keywords
Topological Effect Immunoaffinity Chromatography Supercoiled Plasmid Dyad Symmetry Dyad Symmetry ElementPreview
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