Susceptibility to cytotoxic T lymphocyte-induced apoptosis is a function of the proliferative status of the target

entation of the target cell DNA is unlikely, as the control virusinfected samples did not show oligonudeosomal ladder proteins, nor was the level of spontaneous DNA release different from uninfected target cells. Evaluation of whether HSV-1 infection could directly induce apoptosis revealed that the HSV-1 cytopathic effect kills cells via necrosis (data not shown), consistent with a recent report (24) . In preliminary studies, various RNA viruses, i.e., the coronavirus mouse hepatitis virus, strain A-59, the picornavirus encephalomyocarditis virus, and LCMV, were unable to render the quiescent targets more susceptible to CTL-induced apoptosis, nor did they stimulate DNA synthesis in these cells. However, vaccinia virus, a DNA virus that encodes its own DNA topoisomerase I and other proteins that interact with cell cycle progression factors (25) , increased the susceptibility of quiescent targets to CTL-induced apoptosis.