Bohórquez José Alejandro, Jagannath Chinnaswamy, Xu Huanbin, Wang Xiaolei, Yi Guohua
Department of Cellular and Molecular Biology, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Center for Biomedical Research, The University of Texas Health Science Center at Tyler, Tyler, TX 75708, USA.
Vaccines (Basel). 2024 Aug 9;12(8):901. doi: 10.3390/vaccines12080901.
Coinfection with () and the human immunodeficiency virus (HIV) is a significant public health concern. Individuals infected with who acquire HIV are approximately 16 times more likely to develop active tuberculosis. T cells play an important role as both targets for HIV infection and mediators of the immune response against both pathogens. This review aims to synthesize the current literature and provide insights into the effects of HIV/ coinfection on T cell populations and their contributions to immunity. Evidence from multiple in vitro and in vivo studies demonstrates that T helper responses are severely compromised during coinfection, leading to impaired cytotoxic responses. Moreover, HIV's targeting of -specific cells, including those within granulomas, offers an explanation for the severe progression of the disease. Herein, we discuss the patterns of differentiation, exhaustion, and transcriptomic changes in T cells during coinfection, as well as the metabolic adaptations that are necessary for T cell maintenance and functionality. This review highlights the interconnectedness of the immune response and the pathogenesis of HIV/ coinfection.
[病原体名称]与人类免疫缺陷病毒（HIV）的合并感染是一个重大的公共卫生问题。感染了[病原体名称]的个体感染HIV后，患活动性结核病的可能性大约高出16倍。T细胞作为HIV感染的靶标以及针对这两种病原体的免疫反应介质发挥着重要作用。本综述旨在综合当前文献，深入探讨HIV/[病原体名称]合并感染对T细胞群体的影响及其对免疫的贡献。多项体外和体内研究的证据表明，合并感染期间辅助性T细胞反应严重受损，导致细胞毒性反应受损。此外，HIV对[病原体名称]特异性细胞（包括肉芽肿内的细胞）的靶向作用，为该疾病的严重进展提供了解释。在此，我们讨论合并感染期间T细胞的分化、耗竭和转录组变化模式，以及T细胞维持和功能所必需的代谢适应。本综述强调了免疫反应与HIV/[病原体名称]合并感染发病机制之间的相互联系。
