The observed differences in atherosclerosis burden between HIVposEVs -and HIVnegEVs-treated apoE−/− mice, together with the lack of differences in atherosclerosis burden between HIV PLdepEVs- and PBS-treated apoE−/− mice, suggest that EVs, rather than other factors in the plasma such as lipid proteins, serve as the primary carriers for the atherogenic signals associated with HIV infection. This evidence concerns the gene APOE and HIV infectious disease.