HIV infection is associated with a substantially increased risk of CVD that is not fully accounted for by traditional risk factors. Several lines of evidence suggest that chronic immune cell activation may be complicit. In support of this concept, we recently used 18F-FDG-PET/CT to demonstrate that HIV-infected individuals have increased arterial inflammation compared to non-HIV, FRS-matched controls and that the degree of arterial inflammation is related to markers of monocyte activation. Further, we and others have shown that increased arterial FDG uptake predicts future CVD events in non-HIV cohorts. Together, these observations support the concept that targeting arterial inflammation may provide benefit for HIV infected individuals.