Figure 1.

Model for HIV-1 infection and NLRP3 inflammasome activation to drive atherosclerosis. A model is shown in which HIV-1 infection of a CD4+ T cell can stimulate the NLRP3 inflammasome. This results in IL-1β secretion which impacts on various cell types including endothelial cells, macrophages, monocytes, and smooth muscle, signaling through soluble factors including chemokines, cytokines, adhesion molecules, matrix metalloproteinases. The activation of these factors can potentiate progression of atherosclerotic disease.