Induction of apoptosis by herpes simplex virus in Jurkat cells is partly through caspase-3, -8 and -9 activation.

Herpes simplex virus (HSV), a large DNA containing virus, is endemic in all human populations investigated. After infection of mucocutaneuos surfaces, HSV establishes a latent infection in nerve cells. Various immune evasion mechanisms have been shown to be utilized by HSV including apoptosis induction in Tlymphocytes. However, the mechanisms of T cell infection and apoptosis by HSV are still unknown. The present study investigated the molecular mechanisms of apoptosis induction in T cells by HSV The Jurkat T cell line was used as a representative for T cells. Apoptosis detection by Annexin Vassay demonstrated that both HSV-1 and HSV-2 induced apoptosis in Jurkat cells and caspase-3, -8, and -9 inhibitors blocked apoptosis induced by HSV-1 and HSV-2. The data suggested that HSV-1 and HSV-2 induced apoptosis in T lymphocytes by caspase-dependent pathway. However, apoptosis may occur through other mechanism(s) since caspase inhibitors used in the present study could not completely inhibit apoptosis induced by HSV infection. In addition, the data demonstrated that the number of apoptotic cells induced by HSV-2 was significantly higher than byHSV-1 at 12 hour post-infection (h p.i.) (p = 0.003). Further studies in peripheral blood T cells and the proteins of viruses involved in apoptosis induction should be further performed in order to elucidate the molecular mechanisms of apoptosis induced by these viruses.