Varicella-zoster virus induces apoptosis in cell culture.
Apoptosis is an active mechanism of cell death which can be initiated in response to various stimuli including virus infections. In this work, we demonstrate that lytic infection by varicella-zoster virus (VZV), a human herpesvirus, is characterized by nuclear fragmentation of DNA into oligonucleosomal fragments and by chromatin condensation. In vitro, VZV-induced cell death is actually mediated by apoptosis. The mechanisms developed by cells to protect themselves against apoptosis could be one of the parameters allowing the establishment of virus latency. In the case of VZV, which can remain latent in sensory ganglia, we have not yet identified a cellular or viral protein which could play this protective role, since the observed apoptosis mechanism seems to be independent from Bcl-2, the most frequently described inhibitor of apoptosis.
Sadzot-Delvaux
C
C
Department of Microbiology, University of Liège, Belgium.
Thonard
P
P
Schoonbroodt
S
S
Piette
J
J
Rentier
B
B
D000818:Animals; D017209:Apoptosis; D001483:Base Sequence; D002460:Cell Line; D002522:Chlorocebus aethiops; D004249:DNA Damage; D017931:DNA Primers; D014645:Herpesvirus 3, Human / Q000502:physiology*; D006801:Humans; D008969:Molecular Sequence Data; D011518:Proto-Oncogene Proteins / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2; D051381:Rats; D014407:Tumor Cells, Cultured; D014709:Vero Cells
D017931:DNA Primers; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2