The studies demonstrated elevated ASCVD risk in HIV-1-infected African populations in the presence of cART (NRTIs or NNRTIs) and metabolic syndrome. We have also described the mechanisms of the pathogenesis of metabolic syndrome through the HIV and cART pathways. Our results suggest that the main culprit for the increased ASCVD risk is the virus itself with cART and metabolic syndrome playing an amplifying role as also attested by Rider.223 Also, a study of ‘elite controllers’ – HIV-infected people who control HIV replication to undetectable levels without antiretroviral therapy – showed increased coronary atherosclerosis and monocyte activation compared to uninfected individuals239 suggesting that the main cause of this comorbidity is related to HIV infection itself. Since cARTs are focused at preventing HIV-1 to replicate but not integrating HIV-1 DNA nor are they capable of eliminating long-lived cells that harbor these integrants, it is defintely clear that virus production persists indefinitely even with effective long-term adherence to cART. Moreover, in their study on HIV-1 elite controllers comparing transient controllers – those who lose viral control – with persistent controllers – those who maintain viral control, Tarancon-Diez and colleagues240 found differences in their immunometabolism suggesting that targeting immunometabolism in therapeutic strategies for HIV-1 infection could reduce atherosclerotic cardiovascular risk in HIV-1-infected populations by enhancing immune response and thus clearing HIV-1 from their reservoirs.