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.
This study was supported by the Discovery Fund for Eye Research, the Skirball Program in Molecular Ophthalmology, Public Health Service grants to SW (EY11629, and EY12823) and CJ (1P20RR15635), and USDA grants to CJ (2000-02060, 2002-02450, and 2003-02213).