Apoptosis is an active mechanism of cell death which can be initiated
in response to various stimuli including virus infections. In this wor
k, we demonstrate that lytic infection by varicella-zoster virus (VZV)
, a human herpesvirus, is characterized by nuclear fragmentation of DN
A into oligonucleosomal fragments and by chromatin condensation. In vi
tro, VZV-induced cell death is actually mediated by apoptosis. The mec
hanisms developed by cells to protect themselves against apoptosis cou
ld be one of the parameters allowing the establishment of virus latenc
y. 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 t
his protective role, since the observed apoptosis mechanism seems to b
e independent from Bcl-2, the most frequently described inhibitor of a
poptosis.