Vaccinia virus-induced apoptosis in immature B lymphocytes: role of cellular Bcl-2.
Apoptosis is a form of physiological cell death which can be initiated in response to various stimuli including virus infections. We show that vaccinia virus (VV) infection induces apoptosis in an immature B lymphocyte line, WEHI-231. In these cells, several VV-specific proteins were synthesized during the infection, but neither virus production nor viral DNA synthesis were detected. The intracellular levels of the proto-oncogene Bcl-2, which effectively protects cells from programmed cell death, were found to be down-regulated by the VV infection, suggesting that this down-regulation might be involved in the viral induction of apoptosis in WEHI-231 cells. Stable transfectants overexpressing human Bcl-2 were shown to be resistant to the apoptosis produced by the infection, a finding consistent with the proposed role for the down-regulation of endogenous Bcl-2 in VV-induced apoptotic death.
Baixeras
E
E
Centro Nacional de Biotecnología (CSIC), Universidad Autónoma, Cantoblanco, Madrid, Spain.
Cebrián
A
A
Albar
J P
JP
Salas
J
J
Martínez-A
C
C
Viñuela
E
E
Revilla
Y
Y
D000818:Animals; D017209:Apoptosis; D001402:B-Lymphocytes / Q000473:pathology / Q000821:virology*; D002460:Cell Line; D006801:Humans; D051379:Mice; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000502:physiology*; D014162:Transfection; D014616:Vaccinia virus / Q000502:physiology*
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2