To prolong cell viability and facilitate replication, viruses have evolved multiple mechanisms to inhibit the host apoptotic response. Cellular proteases such as caspases and serine proteases are instrumental in promoting apoptosis. Thus, these enzymes are logical targets for virus-mediated modulation to suppress cell death. Four major classes of viral inhibitors antagonize caspase function: serpins, p35 family members, inhibitor of apoptosis proteins, and viral FLICE-inhibitory proteins. Viruses also subvert activity of the serine proteases, granzyme B and HtrA2/Omi, to avoid cell death. The combined efforts of viruses to suppress apoptosis suggest that this response should be avoided at all costs. However, some viruses utilize caspases during replication to aid virus protein maturation, progeny release, or both. Hence, a multifaceted relationship exists between viruses and the apoptotic response they induce. Examination of these interactions contributes to our understanding of both virus pathogenesis and the regulation of apoptotic enzymes in normal cellular functions.

中文翻译：

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凋亡酶的病毒颠覆：逃离死囚牢房。

为了延长细胞活力并促进复制，病毒已经进化出多种机制来抑制宿主细胞凋亡反应。细胞蛋白酶如半胱天冬酶和丝氨酸蛋白酶有助于促进细胞凋亡。因此，这些酶是病毒介导的调节以抑制细胞死亡的合乎逻辑的目标。四大类病毒抑制剂拮抗 c​​aspase 功能：serpins、p35 家族成员、凋亡蛋白抑制剂和病毒 FLICE 抑制蛋白。病毒还会破坏丝氨酸蛋白酶、颗粒酶 B 和 HtrA2/Omi 的活性，以避免细胞死亡。病毒抑制细胞凋亡的共同努力表明，应该不惜一切代价避免这种反应。然而，一些病毒在复制过程中利用半胱天冬酶来帮助病毒蛋白质成熟、子代释放或两者兼而有之。因此，病毒与其诱导的细胞凋亡反应之间存在多方面的关系。对这些相互作用的检查有助于我们了解病毒的发病机制和正常细胞功能中凋亡酶的调节。