Thomson B J
University of Nottingham, Nottingham City Hospital, Nottingham, UK.
Int J Exp Pathol. 2001 Apr;82(2):65-76. doi: 10.1111/j.1365-2613.2001.iep0082-0065-x.
Apoptosis, or programmed cell death, is essential in development and homeostasis in multi-cellular organisms. It is also an important component of the cellular response to injury. Many cells undergo apoptosis in response to viral infection, with a consequent reduction in the release of progeny virus. Viruses have therefore evolved multiple distinct mechanisms for modulating host cell apoptosis. Viruses may interfere with either the highly conserved 'effector' mechanisms of programmed cell death or regulatory mechanisms specific to mammalian cells. In addition to conferring a selective advantage to the virus, the capacity to prevent apoptosis has an essential role in the transformation of the host cell by oncogenic viruses. This article provides a focussed review of apoptosis and illustrates how the study of viruses has informed our understanding of this process. Selected mechanisms by which viral gene products interfere with cell death are discussed in detail and used to illustrate the general principles of the interactions between viruses and apoptosis.
细胞凋亡，即程序性细胞死亡，在多细胞生物的发育和体内平衡中至关重要。它也是细胞对损伤反应的重要组成部分。许多细胞会因病毒感染而发生凋亡，从而导致子代病毒释放减少。因此，病毒进化出了多种不同机制来调节宿主细胞凋亡。病毒可能会干扰程序性细胞死亡中高度保守的“效应器”机制，也可能干扰哺乳动物细胞特有的调节机制。除了赋予病毒选择性优势外，防止细胞凋亡的能力在致癌病毒转化宿主细胞过程中也起着至关重要的作用。本文重点综述了细胞凋亡，并阐述了对病毒的研究如何增进我们对这一过程的理解。文中详细讨论了病毒基因产物干扰细胞死亡的特定机制，并用以说明病毒与细胞凋亡相互作用的一般原理。
