Centre for Integrative Omics Data Science, Yenepoya (Deemed to be University), Mangalore 575018, India.
Center for Systems Biology and Molecular Medicine, Yenepoya Research Centre, Yenepoya (Deemed to be University), Mangalore 575018, India.
Int J Mol Sci. 2022 Jun 24;23(13):7023. doi: 10.3390/ijms23137023.
The fate of a viral infection in the host begins with various types of cellular responses, such as abortive, productive, latent, and destructive infections. Apoptosis, necroptosis, and pyroptosis are the three major types of regulated cell death mechanisms that play critical roles in viral infection response. Cell shrinkage, nuclear condensation, bleb formation, and retained membrane integrity are all signs of osmotic imbalance-driven cytoplasmic swelling and early membrane damage in necroptosis and pyroptosis. Caspase-driven apoptotic cell demise is considered in many circumstances as an anti-inflammatory, and some pathogens hijack the cell death signaling routes to initiate a targeted attack against the host. In this review, the selected mechanisms by which viruses interfere with cell death were discussed in-depth and were illustrated by compiling the general principles and cellular signaling mechanisms of virus-host-specific molecule interactions.
病毒感染在宿主中的命运始于各种类型的细胞反应，如流产性、生产性、潜伏性和破坏性感染。细胞凋亡、坏死性凋亡和细胞焦亡是三种主要的调控细胞死亡机制，在病毒感染反应中发挥关键作用。细胞皱缩、核浓缩、泡状形成和保留膜完整性是坏死性凋亡和细胞焦亡导致的渗透失衡驱动的细胞质肿胀和早期膜损伤的特征。在许多情况下，半胱天冬酶驱动的细胞凋亡被认为是一种抗炎反应，一些病原体劫持细胞死亡信号通路，对宿主发起靶向攻击。在这篇综述中，深入讨论了病毒干扰细胞死亡的选择机制，并通过编译病毒-宿主特异性分子相互作用的一般原则和细胞信号机制进行了说明。
