Wang Qiankun, Shan Liang
Institute of Infectious Diseases, Shenzhen Bay Laboratory, Shenzhen, Guangdong 518000, China.
Division of Infectious Diseases, Department of Medicine, Washington University School of Medicine, Saint Louis, MO, 63110, USA.
Cell Insight. 2024 Jul 19;3(5):100193. doi: 10.1016/j.cellin.2024.100193. eCollection 2024 Oct.
Human immunodeficiency virus (HIV) continues to be a significant global health challenge despite decades of research and advances in treatment. Substantial gaps in our understanding of the mechanisms of HIV pathogenesis and the host immune responses still exist. The interaction between HIV and these immune responses is pivotal in the disease progression to acquired immunodeficiency syndrome (AIDS). Recently, the caspase recruitment domain-containing protein 8 (CARD8) inflammasome has emerged as a crucial factor in orchestrating innate immune responses to HIV infection and exerting a substantial impact on viral pathogenesis. CARD8 restricts viral replication by detecting the activity of HIV protease. Conversely, it also contributes to the depletion of CD4 T cells, a key feature of disease progression towards AIDS. The purpose of this review is to summarize the role of the CARD8 inflammasome in HIV pathogenesis, delving into its mechanisms of action and potential implications for the development of therapeutic strategies.
尽管经过数十年的研究和治疗进展,人类免疫缺陷病毒(HIV)仍然是一项重大的全球健康挑战。我们对HIV发病机制和宿主免疫反应的理解仍存在重大差距。HIV与这些免疫反应之间的相互作用在疾病进展为获得性免疫缺陷综合征(AIDS)的过程中起着关键作用。最近,含半胱天冬酶招募结构域蛋白8(CARD8)炎性小体已成为协调对HIV感染的固有免疫反应并对病毒发病机制产生重大影响的关键因素。CARD8通过检测HIV蛋白酶的活性来限制病毒复制。相反,它也导致CD4 T细胞耗竭,这是疾病进展至AIDS的一个关键特征。本综述的目的是总结CARD8炎性小体在HIV发病机制中的作用,深入探讨其作用机制以及对治疗策略开发的潜在影响。