Currently, non-AIDS comorbidities (cardiovascular disease, non-AIDS-related cancers, liver disease, osteoporosis, etc.) have become an important cause of morbimortality in patients with human immunodeficiency virus type 1 (HIV-1) infection. The elevation of plasma markers of inflammation has been associated with the development of cardiovascular disease and death from all causes. Therefore, there is great interest in elucidating the underlying causes responsible for this persistent inflammatory status. The intestinal barrier disruption associated with HIV-1 infection may favor the passage of gut microbial products into the blood, resulting in immune stimulation. In this article we review the pathogenesis of bacterial translocation and its relevance to HIV-1 infection.