Necroptosis is a lytic form of programmed cell death that involves the swelling and rupture of dying cells. Although several necroptosis-inducing stimuli have been defined, in most cells this pathway is kept in check by the action of the pro-apoptotic protease caspase-8 and the IAP ubiquitin ligases. How and when necroptosis is triggered under physiological conditions therefore remains a persistent question. Because necroptosis likely arose as a defensive mechanism against viral infection, exploration of this question requires a consideration of host-pathogen interactions, and how the sensing of infection could sensitize cells to necroptosis. Here, we will discuss the role of necroptosis in the response to viral infection, consider why the necroptotic pathway has been favored during evolution, and describe emerging evidence for death-independent functions of key necroptotic signaling components.

中文翻译：

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受控爆炸：病原体防御中坏死病的演变。

坏死病是细胞程序性死亡的一种裂解形式，涉及垂死细胞的肿胀和破裂。尽管已经定义了几种诱导坏死病的刺激物，但是在大多数细胞中，该途径通过促凋亡蛋白酶caspase-8和IAP泛素连接酶的作用而受到抑制。因此，在生理条件下如何以及何时触发坏死病仍然是一个持续存在的问题。由于坏死病可能是作为抵抗病毒感染的防御机制而出现的，因此对该问题的探讨需要考虑宿主与病原体之间的相互作用，以及感染的感应如何使细胞对坏死病敏感。在这里，我们将讨论坏死病在病毒感染反应中的作用，考虑为什么在进化过程中赞成坏死病途径，