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.