Caspase 3 activation during herpes simplex virus 1 infection

During herpes simplex virus 1 (HSV-1) infection, apoptosis is initiated by immediate early gene transcription and is later modulated by proteins synthesized in infected cells. We have previously shown that procaspase 3 levels are reduced during HSV-1 replication. We now demonstrate that a replicatio...

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Bibliographic Details
Published in:Virus research 2006-09, Vol.120 (1), p.163-175
Main Authors: Kraft, Rachel M., Nguyen, Marie L., Yang, Xiao-He, Thor, Ann D., Blaho, John A.
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Caspase 3
Caspase 7
Caspases - deficiency
Caspases - genetics
Caspases - metabolism
Cell Line, Tumor
Cercopithecus aethiops
Enzyme Precursors - deficiency
Enzyme Precursors - genetics
Enzyme Precursors - metabolism
HEp-2 and MCF-7 tumor cells
Herpes Simplex - metabolism
Herpes Simplex - pathology
Herpes Simplex - virology
Herpes simplex virus 1
Herpesvirus 1, Human - physiology
Humans
Vero Cells
Virus Assembly
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Summary:During herpes simplex virus 1 (HSV-1) infection, apoptosis is initiated by immediate early gene transcription and is later modulated by proteins synthesized in infected cells. We have previously shown that procaspase 3 levels are reduced during HSV-1 replication. We now demonstrate that a replication-defective HSV-1 recombinant virus which is incapable of packaging viral DNA into capsids activated caspase 3 but retained the ability to prevent the apoptotic process from killing the infected cells. This implies that HSV-1-dependent apoptosis is not merely a response to abortive infection. Maximum accumulation of the active form of caspase 3 accompanied complete HSV-1-dependent apoptosis. Additionally, caspase 7 was found to be activated during HSV-1-dependent apoptosis. Infected MCF-7 cells which ectopically express caspase 3 underwent more efficient apoptosis than their caspase 3-null parental counterparts, confirming that caspase 3 contributes to HSV-1-dependent apoptosis. However, caspase 3 reconstitution did not make the MCF-7 cells as sensitive as HEp-2 cells to HSV-1-dependent apoptosis, suggesting that other cellular factors may be involved in conferring resistance to this process. These results indicate that caspase 3 activation is a consequence of HSV-1 infection and have important implications in our understanding of the interactions of the virus with host cells.
ISSN:0168-1702
1872-7492
DOI:10.1016/j.virusres.2006.03.003