Human cytomegalovirus immediate early proteins upregulate endothelial p53 function.

Infected endothelial cells are found to be resistant to apoptosis possibly mediated by p53 cytoplasmic sequestration. We explored whether the immediate early 84 kDa protein (IE84) of cytomegalovirus (CMV) is responsible for p53 cytoplasmic sequestration. The endothelial cells were transfected with plasmids containing IE1 and 2 coding regions which are known to synthesize IE84 and 72 proteins. Our study found that p53 expression was significantly elevated in endothelial cells transfected with IE1 and 2 plasmids. However, p53 was only found in the nucleus rather than sequestered in the cytoplasm. We have demonstrated that IE84 and 72 are not responsible for p53 dysfunction caused by CMV infection, rather they upregulate p53 function and promote endothelial apoptosis.