Abstract
When the bovine herpesvirus 1 (BHV-1) latency-related (LR) gene is inserted into the latency-associated transcript (LAT) locus of a herpes simplex virus type 1 (HSV-1) LAT deletion mutant, high levels of spontaneous reactivation from latency and enhanced pathogenesis occur. The LR gene, but not LAT, inhibits caspase 3 cleavage during productive infection. Plasmids containing LAT or the LR gene inhibit caspase 3 activation in transiently transfected cells, suggesting productive infection blocks certain antiapoptotic properties of LAT. These studies demonstrate a correlation between the enhanced pathogenic potential of CJLAT and the LR gene inhibiting caspase 3 cleavage during productive infection.
Original language | English |
---|---|
Pages (from-to) | 64-70 |
Number of pages | 7 |
Journal | Journal of NeuroVirology |
Volume | 10 |
Issue number | 1 |
DOIs | |
Publication status | Published - 2004 Feb |
All Science Journal Classification (ASJC) codes
- Neurology
- Clinical Neurology
- Cellular and Molecular Neuroscience
- Virology