Derfuss T, Meinl E
Department of Neuroimmunology, Max Planck Institute of Neurobiology, Martinsried, Germany.
Curr Top Microbiol Immunol. 2002;269:257-72. doi: 10.1007/978-3-642-59421-2_15.
The induction of apoptosis of virus-infected cells is an important defense mechanism of the host. Apoptosis of an infected cell can be induced cell autonomously as a consequence of viral replication or can be mediated by CTLs attacking the infected cells. Herpesviruses have developed different strategies to interfere with cell-autonomous apoptosis and to block CTL-induced apoptosis mediated by death receptors such as Fas and TRAIL. Herpesviruses, which establish a lifelong persistence in the infected host, can be found principally in two different conditions, episomal persistence with a limited number of genes expressed and lytic replication with expression of almost all genes. To meet the need of the virus to enhance survival of the infected cell, herpesviruses have evolved different strategies that function during both episomal persistence and lytic replication. Herpesviruses, which encode 70 to more than 200 genes have incorporated cell homologous antiapoptotic genes, they code for multifunctional genes that can also regulate apoptosis, and, finally, they modulate the expression of cellular apoptosis-regulating genes to favor survival of the infected cells. Viral interference with host cell apoptosis enhances viral replication, facilitates virus spread and persistence, and may promote the development of virus-induced cancer.
诱导病毒感染细胞凋亡是宿主的一种重要防御机制。受感染细胞的凋亡可因病毒复制而被细胞自主诱导，也可由细胞毒性T淋巴细胞（CTL）攻击受感染细胞介导。疱疹病毒已发展出不同策略来干扰细胞自主凋亡，并阻断由死亡受体（如Fas和TRAIL）介导的CTL诱导的凋亡。疱疹病毒在受感染宿主中建立终身潜伏感染，主要可处于两种不同状态：基因表达有限的游离体潜伏状态和几乎所有基因都表达的裂解复制状态。为满足病毒提高受感染细胞存活率的需求，疱疹病毒已进化出在游离体潜伏和裂解复制过程中均起作用的不同策略。编码70至200多个基因的疱疹病毒纳入了细胞同源抗凋亡基因，它们编码多功能基因，这些基因也可调节凋亡，最后，它们调节细胞凋亡调节基因的表达以利于受感染细胞存活。病毒对宿主细胞凋亡的干扰会增强病毒复制，促进病毒传播和持续存在，并可能促进病毒诱导的癌症发展。
