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 (US) |
---|---|
Pages (from-to) | 1500-1503 |
Number of pages | 4 |
Journal | Science |
Volume | 287 |
Issue number | 5457 |
DOIs | |
State | Published - Feb 25 2000 |
ASJC Scopus subject areas
- General