冠状病毒采用多种生存策略，其中内源性或外源性细胞凋亡的激活最为突出，其中病毒蛋白发挥着关键作用。值得注意的是，与低致病性病毒株相比，SARS-CoV-2、SARS-CoV 和 MERS-CoV 等高致病性冠状病毒表现出更多的非结构蛋白，从而促进其通过多种途径诱导细胞凋亡的能力。此外，这些病毒蛋白善于抑制宿主免疫反应，从而增强病毒复制和持久性。这篇综述深入研究了高致病性冠状病毒与细胞凋亡之间复杂的相互作用，系统地阐明了病毒蛋白诱导细胞凋亡的分子机制。此外，它还探索了作为抗病毒药物的细胞凋亡抑制和利用诱导细胞凋亡的病毒蛋白作为治疗方式的潜在治疗途径。这些见解不仅揭示了病毒发病机制，还为癌症治疗提供了新的视角。© 2024。作者。

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.© 2024. The Author(s).