Summary
This NIH research project investigates the mechanisms by which HIV-associated extracellular vesicles containing the Nef protein (Nef EVs) contribute to accelerated atherosclerosis in people living with HIV (PLWH). The study uses a systems biology approach combining multi-omics, data integration, and network analysis to profile macrophage heterogeneity and function. The central hypothesis is that Nef EVs impair efferocytosis (the clearance of dead cells by macrophages), shifting macrophage populations toward an atherogenic phenotype and promoting high-risk atherosclerotic plaque formation. Findings are intended to identify novel therapeutic targets for cardiovascular disease in long-term HIV survivors.
