Mitoquinone Mesylate and Mitochondrial DNA in End Organs in Humanized Mouse Model of Chronic Treated Human Immunodeficiency Virus Infection

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. No treatment exists for mitochondrial dysfunction, a contributor to end-organ disease in human immunodeficiency virus (HIV). The mitochondrial antioxidant mitoquinone mesylate attenuated reduction of mitochondrial DNA as measure of mitochondrial dysfunction in end organs of an animal model of HIV.

Automated summary

Currently, there is no treatment available for mitochondrial dysfunction, which contributes to end-organ disease in HIV patients. The mitochondrial antioxidant MitoQ has been shown to alleviate mitochondrial dysfunction in animal models of various diseases, but its effectiveness in HIV has not been explored. In this study, using a humanized murine model of chronic HIV infection, we found that HIV-1-infected mice treated with antiretroviral therapy and MitoQ had higher levels of mitochondrial DNA compared to HIV-1-infected mice on antiretroviral therapy alone. These findings suggest that MitoQ could be a potential treatment for mitochondrial dysfunction in HIV.