In several cell types, poliovirus activates the apoptotic program, implementation of which is suppressed by viral antiapoptotic functions. In such cells, productive
infection leads to a necrotic cytopathic effect (CPE), while abortive reproduction, associated with inadequate viral antiapoptotic functions, results in apoptosis. Here, we describe two other types of cell response to poliovirus
infection. Murine L20B cells expressing human
poliovirus receptor responded to the
infection by both CPE and apoptosis concurrently. Interruption of productive
infection decreased rather than increased the proportion of apoptotic cells. Productive
infection was accompanied by the early efflux of
cytochrome c from the mitochondria in a proportion of cells and by activation of DEVD-specific
caspases. Inactivation of
caspase-9 resulted in a marked, but incomplete, prevention of the apoptotic response of these cells to
viral infection. Thus, the poliovirus-triggered apoptotic program in L20B cells was not completely suppressed by the viral antiapoptotic functions. In contrast, human
rhabdomyosarcoma RD cells did not develop appreciable apoptosis during productive or abortive
infection, exhibiting inefficient efflux of
cytochrome c from mitochondria and no marked activation of DEVD-specific
caspases. The cells were also refractory to several nonviral apoptosis inducers. Nevertheless, typical
caspase-dependent signs of apoptosis in a proportion of RD cells were observed after cessation of viral reproduction. Such "late" apoptosis was also observed in productively infected HeLa cells. In addition, a tiny proportion of all studied cells were TUNEL positive even in the presence of a
caspase inhibitor. Degradation of
DNA in such cells appeared to be a postmortem phenomenon.
Biological relevance of variable host responses to
viral infection is discussed.