Volume 39 (2014) Issue 6 Pages 909-917
Virus infection has been shown to accelerate atherosclerosis. Serological studies indicate a link between the Herpes simplex virus (HSV) infection and atherosclerosis, which is initiated and progression of which is promoted by such factors as oxidized low-density lipoprotein (ox-LDL)-induced endothelial dysfunction. In order to recognize the direct role of HSV-2 in endothelial dysfunction, the present study investigated the infection of HSV-2 in endothelial ECV304 cells and the induction of cell apoptosis in the presence of ox-LDL. We firstly examined the HSV-2 infection by immunohistochemical assay for viral gB protein, quantitative PCR for viral ICP4 mRNA, or via virus growth determination. Then we investigated the regulation of HSV-2 infection on the cell viability and apoptosis, in the absence or presence of ox-LDL. In addition, we analyzed the apoptosis-associated molecules in the HSV-2-infected ECV304 cells. The results demonstrated that HSV-2 infected endothelial ECV304 cells and replicated efficiently, and the virus infection significantly reduced the cell viability and significantly induced cell apoptosis; particularly, cell viability reduction and cell apoptosis induction were aggravated by the ox-LDL presence. Moreover, the western blot assay confirmed the apoptosis induction; there was a significantly high level of released cytochrome c, activated caspase 3 and lyzed Poly (ADP-ribose) polymerase (PARP) by the activated caspase 3 in the HSV-2-infected ECV304 cells, particularly the cells subject to ox-LDL. Thus, we confirmed that HSV-2 infected endothelial ECV304 cells, induced cell apoptosis, which was aggravated by ox-LDL.