Department of Medicine, Division of Infectious Diseases, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
J Infect Dis. 2023 Jun 28;228(1):59-63. doi: 10.1093/infdis/jiad044.
No treatment exists for mitochondrial dysfunction, a contributor to end-organ disease in human immunodeficiency virus (HIV). The mitochondrial antioxidant mitoquinone mesylate (MitoQ) attenuates mitochondrial dysfunction in preclinical mouse models of various diseases but has not been used in HIV. We used a humanized murine model of chronic HIV infection and polymerase chain reaction to show that HIV-1-infected mice treated with antiretroviral therapy and MitoQ for 90 days had higher ratios of human and murine mitochondrial to nuclear DNA in end organs compared with HIV-1-infected mice on antiretroviral therapy. We offer translational evidence of MitoQ as treatment for mitochondrial dysfunction in HIV.
目前尚无针对线粒体功能障碍的治疗方法，而线粒体功能障碍是人类免疫缺陷病毒 (HIV) 导致终末器官疾病的一个因素。线粒体抗氧化剂甲磺酰甲烷米托醌 (MitoQ) 可减轻各种疾病的临床前小鼠模型中的线粒体功能障碍，但尚未在 HIV 中使用。我们使用慢性 HIV 感染的人源化小鼠模型和聚合酶链反应表明，与接受抗逆转录病毒治疗的 HIV-1 感染小鼠相比，接受抗逆转录病毒治疗和 MitoQ 治疗 90 天的 HIV-1 感染小鼠的终末器官中人类和鼠线粒体与核 DNA 的比值更高。我们提供了 MitoQ 作为 HIV 中线粒体功能障碍治疗的转化证据。
