抄録
Viral infection often causes the death of host cells, and this phenomenon, called the cytopathic effect, has been thought to occur when the replicated virus particles leave the cells. However, some viruses appear to bring about the prolonged survival of host cells. Now we know that these phenomena involve the regulation of apoptosis; the cytopathic effect reflects the induction of host cell apoptosis and the inhibition of apoptosis causes host cells to survive. These events apparently require the function of both viral and cellular genes, which encode either apoptosis-inducing or -inhibiting proteins. The prolonged survival of the host cell is presumably beneficial for the virus to produce more progenitors, whereas the earlier death of virus-infected cells could result in protecting the organism from viral diseases. It is thus postulated that the induction of apoptosis is a self-defense mechanism of the host, while the inhibition of apoptosis is a consequence of viral action countering the host response. In this review, the mechanism underlying the regulation of apoptosis in virus-infected cells is outlined and the implications of the findings are discussed.
