Mitoquinone Mesylate and Mitochondrial DNA in End Organs in Humanized Mouse Model of Chronic Treated Human Immunodeficiency Virus Infection.
Sihyeong SongSandro SattaMadhav B SharmaCristelle HugoAthanassios KossyvakisShubhendu Sen RoyTheodoros KelesidisPublished in: The Journal of infectious diseases (2023)
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.
Keyphrases
- antiretroviral therapy
- hiv infected
- human immunodeficiency virus
- hiv positive
- hiv infected patients
- hiv aids
- mouse model
- mitochondrial dna
- endothelial cells
- oxidative stress
- induced pluripotent stem cells
- high fat diet induced
- copy number
- stem cells
- combination therapy
- insulin resistance
- dna methylation
- metabolic syndrome
- gene expression
- skeletal muscle
- hiv testing
- men who have sex with men
- pluripotent stem cells
- replacement therapy
- chronic myeloid leukemia
- circulating tumor cells