Highly active antiretroviral therapy (HAART) has greatly reduced the risk of early death from opportunistic infections and extended the lifespan of people infected with the human immunodeficiency virus (HIV). Thus, many complications and organic damage in the HIV-infected population emerge. Cardiovascular disease as coronary artery disease has become a matter of particular concern. Its incidence is greatly increased in the HIV-infected population over that of people of the same age in the absence of general cardiovascular risk factors. Despite several clinical and laboratory studies in the association between HIV infection and cardiovascular disease, the pathogenic mechanisms of this significant clinical problem are largely unknown and are now under active investigation. Endothelial dysfunction is possibly the most plausible link between HIV infection and atherosclerosis. Increased expression of adhesion molecules such as intercellular adhesion molecule (ICAM)-1 and endothelial adhesion molecule (E-selectin) and inflammatory cytokines such as tumor necrosis factor (TNF)-alpha and interleukin (IL-6 has been reported in HIV-positive patients. The effect of HAART on endothelial function in HIV-positive patients is also demonstrated. In this review, we focus on the recent research update of HIV-associated vascular disease and vascular injury. We analyze and discuss the recent clinical and laboratory investigations on the effect of HIV, viral protein, and HAART therapy on endothelial injury and vascular disease; identify the areas of controversy and clinical relevance; and suggest some directions for future research.