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| Content Provider | PubMed Central |
|---|---|
| Author | Everett, R. D. Orr, A. Preston, C. M. |
| Abstract | The ability of herpes simplex virus type 1 (HSV-1) to attain a latent state in sensory neurones and reactivate periodically is crucial for its biological and clinical properties. The active transcription of the entire 152 kb viral genome during lytic replication contrasts with the latent state, which is characterized by the production of a single set of nuclear-retained transcripts. Reactivation of latent genomes to re-initiate the lytic cycle therefore involves a profound change in viral transcriptional activity, but the mechanisms by which this fundamentally important process occurs are yet to be well understood. In this report we show that the stimulation of the onset of viral lytic infection mediated by the viral immediate-early (IE) protein Vmw110 is strikingly inhibited by inactivation of the ubiquitin-proteasome pathway. Similarly, the Vmw110-dependent reactivation of quiescent viral genomes in cultured cells is also dependent on proteasome activity. These results constitute the first demonstration that the transcriptional activity of a viral genome can be regulated by protein stability control pathways. |
| Related Links | http://dx.doi.org/10.1093/emboj/17.24.7161 |
| Ending Page | 7169 |
| Page Count | 9 |
| Starting Page | 7161 |
| File Format | |
| ISSN | 14602075 |
| e-ISSN | 14602075 |
| Journal | The EMBO Journal |
| Issue Number | 24 |
| Volume Number | 17 |
| Language | English |
| Publisher Date | 1998-12-15 |
| Access Restriction | Open |
| Subject Keyword | Biochemistry, Genetics and Molecular Biology(all) Immunology and Microbiology(all) Neuroscience(all) Molecular Biology Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Neuroscience Immunology and Microbiology Medicine Molecular Biology |
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