Mechanisms of dengue virus-induced cell death.
The outcome of virus infection depends on viral and host factors. The interactions between flaviviruses and their target cells must be investigated if we are to understood the pathogenicity of these RNA viruses. Host cells are thought to respond to viral infection by initiation of apoptotic cell death. Apoptosis is an active process of cellular self-destruction with distinctive morphological and biochemical features. There is mounting evidence that dengue (DEN) virus can trigger the host cell to undergo apoptosis in a cell-dependent manner. Virally induced apoptosis contributes directly to the cytopathogenic effects of DEN virus in cultured cells. The induction of apoptosis involves the activation of intracellular signaling systems. Although the underlying molecular processes that trigger apoptosis are not well characterized, our knowledge regarding the cellular mechanisms and viral determinants of the outcome of DEN virus infection of target cells is improving. The cellular factors that regulate cell death, such as Bcl-2 family members, can modulate the outcome of DEN virus infection in cultured cells. Apoptosis inhibitors delay DEN virus-induced apoptosis, thereby providing a suitable environment for the virus. During DEN virus infection, cell death is also modulated by the virulence of the infecting strains. The purpose of this review is to present recent information on the cellular mechanisms and viral proteins associated with apoptosis in response to DEN virus. This knowledge may provide new insights into the viral pathogenicity.
Courageot
Marie-Pierre
MP
Unité Postulante des Interactions Moléculaires Flavivirus-Hôtes, Virology Department, Pasteur Institute, 75724 Paris, France.
Catteau
Adeline
A
Desprès
Philippe
P
D000818:Animals; D017209:Apoptosis; D003715:Dengue / Q000473:pathology; D003716:Dengue Virus / Q000472:pathogenicity*; D006801:Humans; D016328:NF-kappa B / Q000502:physiology; D009336:Necrosis; D018384:Oxidative Stress; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D015398:Signal Transduction; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53