RESUMO
Human cytomegalovirus (HCMV) is an important opportunistic pathogen in immunocompromised individuals and is recognized as a major viral cause of birth defects. HCMV has the ability to establish lifelong persistence and latent infection following primary exposure. Apoptosis is an innate cellular defense response to viral infection. HCMV can block apoptosis in various cell types. Here we show that HCMV promotes survival of human embryonic lung fibroblasts by activating of MAPK/ERK signaling pathway. Bag-1 is up-regulated in a MAPK/ERK-dependent fashion in infected cells. Depletion of Bag-1 suppresses the antiapoptotic effect of HCMV. Taken together, these data indicate that Bag-1 up-regulation is required to maintain apoptosis resistance in HCMV infected cells.