Metal Pollution as a Risk Factor for HIV Infection

The human C-C chemokine receptor type 5 (CCR5) is a molecule primarily expressed on the surface of inflammatory cells, acting as the main HIV co-receptor. In order to penetrate host cells, HIV interacts with both CCR5 and the CD4 molecule during the infectious process. Emerging evidence suggests that pollution by metals, such as aluminum, lead, and manganese, triggers CCR5-mediated inflammation, which may have important implications for the risk of HIV infection. Specifically, we hypothesize that exposure to pollution by metals causes inflammation and elevated CCR5 expression on the surface of CD4+ cells, resulting in an increased risk of HIV infection. Our hypothesis is supported by toxicogenomic data, which shows that both air pollutants and some metals (e.g., arsenic, cadmium, nickel) induce CCR5 expression. Finally, approaches to evaluate the hypothesis are suggested. If confirmed, our hypothesis introduces environmental pollution to the set of biological factors influencing the risk of HIV infection.