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Abstract：
Bcl-xL represents a family of proteins responsible for the regulation of the intrinsic apoptosis pathway. Due to its anti-apoptotic activity, Bcl-xL co-determines the viability of various virally infected cells. Their survival may determine the effectiveness of viral replication and spread, dynamics of systemic infection, and viral pathogenesis. In this paper, we have reviewed the role of Bcl-xL in the context of host infection by eight different RNA and DNA viruses: hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV), influenza A virus (IAV), Epstein-Barr virus (EBV), human T-lymphotropic virus type-1 (HTLV-1), Maraba virus (MRBV), Schmallenberg virus (SBV) and coronavirus (CoV). We have described an influence of viral infection on the intracellular level of Bcl-xL and discussed the impact of Bcl-xL-dependent cell survival control on infection-accompanying pathogenic events such as tissue damage or oncogenesis. We have also presented anti-viral treatment strategies based on the pharmacological regulation of Bcl-xL expression or activity.
摘要：
Bcl-xL代表负责调节内在凋亡途径的蛋白质家族。由于其抗凋亡活性，Bcl-xL共同决定各种病毒感染细胞的生存力。它们的存活可能决定病毒复制和传播的有效性，全身感染的动力学，和病毒的发病机制。在本文中,我们回顾了Bcl-xL在八种不同的RNA和DNA病毒宿主感染的背景下的作用：乙型肝炎病毒（HBV），丙型肝炎病毒（HCV），人类免疫缺陷病毒（HIV），甲型流感病毒（IAV），EB病毒(EBV)人类嗜T淋巴细胞病毒1型（HTLV-1），马拉巴病毒(MRBV),施马伦贝格病毒(SBV)和冠状病毒(CoV)。我们已经描述了病毒感染对Bcl-xL细胞内水平的影响，并讨论了Bcl-xL依赖性细胞存活控制对伴随感染的致病事件如组织损伤或肿瘤发生的影响。我们还提出了基于Bcl-xL表达或活性的药理学调节的抗病毒治疗策略。
