PDF(Pubmed)
Abstract：
Coronaviruses employ various strategies for survival, among which the activation of endogenous or exogenous apoptosis stands out, with viral proteins playing a pivotal role. Notably, highly pathogenic coronaviruses such as SARS-CoV-2, SARS-CoV, and MERS-CoV exhibit a greater array of non-structural proteins compared to low-pathogenic strains, facilitating their ability to induce apoptosis via multiple pathways. Moreover, these viral proteins are adept at dampening host immune responses, thereby bolstering viral replication and persistence. This review delves into the intricate interplay between highly pathogenic coronaviruses and apoptosis, systematically elucidating the molecular mechanisms underpinning apoptosis induction by viral proteins. Furthermore, it explores the potential therapeutic avenues stemming from apoptosis inhibition as antiviral agents and the utilization of apoptosis-inducing viral proteins as therapeutic modalities. These insights not only shed light on viral pathogenesis but also offer novel perspectives for cancer therapy.
摘要：
冠状病毒采用各种生存策略，其中内源性或外源性凋亡的激活突出，病毒蛋白起着关键作用。值得注意的是,高致病性冠状病毒，如SARS-CoV-2，SARS-CoV，与低致病性菌株相比，MERS-CoV表现出更多的非结构蛋白，促进它们通过多种途径诱导细胞凋亡的能力。此外，这些病毒蛋白擅长抑制宿主的免疫反应，从而支持病毒复制和持久性。这篇综述探讨了高致病性冠状病毒与细胞凋亡之间复杂的相互作用。系统地阐明病毒蛋白诱导凋亡的分子机制。此外，它探讨了潜在的治疗途径，源于凋亡抑制作为抗病毒剂和利用诱导凋亡的病毒蛋白作为治疗方式。这些见解不仅阐明了病毒的发病机理，而且为癌症治疗提供了新的视角。
