Md. A. Hossain, Jinsun Kim, Faysal Bin Hamid and Cha-Gyun Shin
Department of Systems Biotechnology, Chung-Ang University, South Korea
Foamy virus infection induces cytopathology in several cell types from different species. The exact mechanism of cell killing by foamy viruses is still unknown. In this study, we have investigated the mechanism of cell death induced by prototype foamy virus (PFV) infection in baby hamster kidney (BHK 21) cells lines. PFV induces apoptosis by exhibiting morphological alterations such as chromatin condensation, blebbing, and nuclear fragmentation. In addition, PFV infection causes the fragmentation of chromosomal DNA, upregulation of Bax, and activation of caspases-3. Upregulation of Bax initiates the translocation of cytochrome-c from mitochondria to the cytoplasm, suggesting that PFVinduced apoptosis is triggered predominantly via the mitochondrial mediated pathway. Blocking apoptosis using caspases inhibitors increased PFV-infected BHK 21 cell viability. Although blocking apoptosis resulted in reduced progeny release, maximal accumulation of PFV was found in apoptosis-blocked cells. This report provides the first systematic experimental account of the mechanism of apoptosis induced by PFV infection, which will provide valuable insights for understanding why pathology is not associated in animals infected with cytopathic foamy viruses.
Keywords: Apoptosis, prpototype foamy virus.