Thanks to the efficacy of combination antiretroviral therapy (cART), human immunodeficiency virus (HIV) infection, once considered a terminal diagnosis, has transformed into a chronic, manageable condition. Consequently, mortality from opportunistic infections has significantly declined, with cardiovascular disease now emerging as the leading cause of death among people living with HIV (PLWH). Along with traditional risk factors like smoking, dyslipidemia, metabolic syndrome, and combination antiretroviral therapy (cART), HIV-encoded proteins have emerged as direct etiologies of cardiovascular pathology. These viral proteins have been shown to exert pathogenic effects through mechanisms that result in endothelial activation, chronic inflammation, oxidative stress, and vascular remodeling. Although many studies have investigated the direct effects of these viral proteins on cells in culture, the pathophysiological relevance of the alterations reported often remains to be established in an in vivo setting. This mini-review provides a brief overview of the role of these proteins in HIV-related cardiovascular (CV) complications.