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| Content Provider | PubMed Central |
|---|---|
| Author | Sinclair, A. J. Brimmell, M. Farrell, P. J. |
| Abstract | BZLF1 repression of transcription from the Epstein-Barr virus BC-R2 promoter (Cp) was shown to require a glucocorticoid response element in cis and glucocorticoids in trans. The mechanism of the repression is indirect and involves up regulation of the cellular c-fos proto-oncogene. Glucocorticoids maintain Epstein-Barr virus latency, and removal of glucocorticoids from the cell culture medium results in activation of the productive cycle. This inverse regulation of the expression of latent and productive cycle genes contributes to the switch between virus latency and the productive cycle. Glucocorticoid control of BC-R2 might also provide a mechanism for EBNA promoter switching during early infection and in development of the restricted latent pattern of gene expression. |
| Starting Page | 70 |
| File Format | |
| ISSN | 10985514 |
| e-ISSN | 10985514 |
| Journal | Journal of Virology |
| Issue Number | 1 |
| Volume Number | 66 |
| Language | English |
| Publisher Date | 1992-01-01 |
| Access Restriction | Open |
| Subject Keyword | Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Virology Immunology Microbiology Insect Science |
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