Figure 2.

HIV infection leads to increases in TGF-β1 levels, which may induce pathologic cardiac fibrosis. Active TGF-β1 upregulation can occur through various mechanisms, including direct binding of HIV envelope to platelets, induction of IL-6 and IL-8 and induction of tissue factor and reactive oxygen species (ROS). Other cells involved in this inflammatory milieu, may also contribute to TGF-β release. cART may mitigate, but not abolish, these perturbations. In addition, certain antiretroviral therapies, particularly those based on protease inhibitors, may accelerate cardiac fibrosis via direct activation of platelets. Metabolic disturbances linked to HIV and certain cART regimens may contribute to these pathological processes as, for example, cART-linked hyperlipidaemia can activate platelets. cART, combination antiretroviral therapy; TGF-β, transforming growth factor β.