Abstract
Latent infections with periodic reactivation are a common outcome after acute infection with many viruses. The latency-associated transcript (LAT) gene is required for wild-type reactivation of herpes simplex virus (HSV). However, the underlying mechanisms remain unclear. In rabbit trigeminal ganglia, extensive apoptosis occurred with LAT- virus but not with LAT+ viruses. In addition, a plasmid expressing LAT blocked apoptosis in cultured cells. Thus, LAT promotes neuronal survival after HSV-1 infection by reducing apoptosis.
| Original language | English |
|---|---|
| Pages (from-to) | 1500-1503 |
| Number of pages | 4 |
| Journal | Science |
| Volume | 287 |
| Issue number | 5457 |
| DOIs | |
| Publication status | Published - 2000 Feb 25 |
All Science Journal Classification (ASJC) codes
- General
Fingerprint
Dive into the research topics of 'Virus-induced neuronal apoptosis blocked by the herpes simplex virus latency-associated transcript'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver