Veterinary and Biomedical Sciences, Department of


Date of this Version

December 2007


Published in Virology 369:1 (December 5, 2007), pp. 12-18; doi:10.1016/j.virol.2007.07.023 Copyright © 2007 Elsevier Inc. Used by permission.


The herpes simplex virus type 1 (HSV-1) latency associated transcript (LAT) gene’s anti-apoptosis activity plays a central, but not fully elucidated, role in enhancing the virus’s reactivation phenotype. In transient transfection experiments, LAT increases cell survival following an apoptotic insult in the absence of other HSV-1 genes. However, the high background of untransfected cells has made it difficult to demonstrate that LAT inhibits specific apoptotic factors such as caspases. Here we report that, in mouse neuroblastoma cell lines (C1300) stably expressing high levels of LAT, cold shock induced apoptosis was blocked as judged by increased survival, protection against DNA fragmentation (by DNA ladder assay), and inhibition of caspase 3 cleavage and activation (Western blots).