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Use of antiretroviral therapy has markedly reduced morbidity and mortality associated with human immunodeficiency virus (HIV) infection. Nonetheless, all-cause mortality rates remain high in HIV-infected patients compared to the general population, with non-AIDS conditions comprising almost half of deaths. Rates of coronary artery disease (CHD) are over twice as high in HIV-infected compared to matched uninfected controls, with rates anticipated to increase as this population ages. Factors contributing to increased risk of CHD in HIV-infected patients remain to be clearly elucidated. While some studies have strongly suggested that hepatitis C (HCV) co-infection is associated with increased rates of CHD in HIV-infected patients, results in all studies have not been consistent. Since HIV, HCV, and atherosclerosis are all associated with chronic inflammation and immune activation, it can be challenging to understand relative disease pathogenesis when found concurrently in individual patients. Identifying predictors of CHD progression from overlapping pathways has the potential to suggest novel preventive and therapeutic intervention strategies to mitigate CHD progression. In addition, if HCV infection is confirmed to confer additional risk for CHD among HIV-infected patients, this would provide further justification to treat HCV early and aggressively in this population irrespective of liver fibrosis stage.The presentation will review the data on the individual contribution of HIV and chronic hepatitis C infection on the development of cardiovascular disease and the proposed mechanisms for these observations. Finally, new research investigating the intersections of these three disease processes with potential for future preventive and therapeutic interventions will be discussed.