Kovacs Laszlo, Khakina Beryl N, Belin de Chantemèle Eric J
Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, Georgia, United States.
Division of Pulmonary, Critical Care, & Sleep Medicine, Department of Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, United States.
Am J Physiol Cell Physiol. 2025 Aug 1;329(2):C592-C598. doi: 10.1152/ajpcell.00379.2025. Epub 2025 Jul 11.
Thanks to the efficacy of combination antiretroviral therapy (cART), human immunodeficiency virus (HIV) infection, once considered a terminal diagnosis, has transformed into a chronic, manageable condition. Consequently, mortality from opportunistic infections has significantly declined, with cardiovascular disease now emerging as the leading cause of death among people living with HIV (PLWH). Along with traditional risk factors like smoking, dyslipidemia, metabolic syndrome, and combination antiretroviral therapy (cART), HIV-encoded proteins have emerged as direct etiologies of cardiovascular pathology. These viral proteins have been shown to exert pathogenic effects through mechanisms that result in endothelial activation, chronic inflammation, oxidative stress, and vascular remodeling. Although many studies have investigated the direct effects of these viral proteins on cells in culture, the pathophysiological relevance of the alterations reported often remains to be established in an in vivo setting. This mini-review provides a brief overview of the role of these proteins in HIV-related cardiovascular (CV) complications.
多亏了联合抗逆转录病毒疗法（cART）的疗效，曾经被视为绝症的人类免疫缺陷病毒（HIV）感染已转变为一种可慢性管理的疾病。因此，机会性感染导致的死亡率显著下降，心血管疾病现已成为HIV感染者（PLWH）的主要死因。除了吸烟、血脂异常、代谢综合征和联合抗逆转录病毒疗法（cART）等传统风险因素外，HIV编码的蛋白质已成为心血管病理的直接病因。这些病毒蛋白已被证明通过导致内皮细胞活化、慢性炎症、氧化应激和血管重塑的机制发挥致病作用。尽管许多研究调查了这些病毒蛋白对培养细胞的直接影响，但所报道的改变在体内环境中的病理生理相关性往往仍有待确定。本综述简要概述了这些蛋白在HIV相关心血管（CV）并发症中的作用。
