Co-infections with other viral or bacterial pathogens may increase CVD risk by enhancing HIV-associated immune activation and inflammation or through direct effects on the vascular endothelium. The best studied of these pathogens is cytomegalovirus (CMV), which can activate endothelial cells, promote inflammation and has been associated with serious non-AIDS events, including CVD [52]. As yet, there is no evidence-based strategy to modify CMV infection in people with HIV infection receiving ART, with no available vaccine and no studies to date indicating that antiviral therapy (eg. valganciclovir) is a means of reducing CVD risk.
Co-infection with hepatitis C virus (HCV) has also been associated with increased rates of CVD [53], although the specific benefits of treatment for HCV infection on CVD has not been established to date [54]