Chronic immune activation and inflammation are associated with an increased risk of atherosclerosis in HIV-infected patients. In this review, we discuss the role of established and novel imaging modalities to define more accurately the structure and function of inflammation-mediated atherosclerosis in the context of HIV. Historically, carotid ultrasound studies were the first to show higher rates of subclinical atherosclerosis in HIV-infected subjects versus uninfected controls. However, computed tomography is the noninvasive gold standard for imaging the coronary arteries, and studies in HIV suggest a higher prevalence of noncalcified plaque. Endothelial dysfunction can be quantified by measuring flow-mediated brachial artery dilation by ultrasound and has been used extensively in antiretroviral switching trials and small pilot trials of therapeutics to assess cardiovascular risk in this population. In the future, novel imaging modalities such as intracoronary optical coherence tomography, positron emission tomography imaging of 18F-fluorodeoxyglucose uptake, and molecular-targeted magnetic resonance imaging will characterize the burden of vulnerable plaque and other unique features of inflammatory atherosclerosis in HIV.