PROJECT SUMMARY/ABSTRACT As a sleep-medicine physician, I seek to understand how sleep health affects the progression and long-term consequences of chronic disease and, ultimately, implement sleep-based interventions to improve the health of patients. Sleep disorders are highly prevalent among people with HIV (PWH), and emerging evidence suggests that sleep disorders may increase the risk of cardiovascular disease in PWH. Sleep disorders, such as obstructive sleep apnea (OSA) and insufficient sleep duration, are recognized as indepdent risk factors for cardiovascular risk. However, little is known about how sleep disorders worsen chronic inflammation among PWH. One understudied pathway by sleep disorders may increase inflammation and cardiovascular risk is by promoting monocyte activation. PWH experience chronic monocyte dysregulation despite antiretroviral therapy, and those with a greater burden of monocyte activation are at an higher risk of developing cardiovascular disease. Monocytes from individuals exposed to OSA or insufficient sleep exhibit markers of monocyte activation, such as greater production of proinflammatory cytokines and expression of cellular adhesion markers. Various stimuli have been found to contribute to excessive monocyte activation, but the impact of sleep disorders on monocyte activation in PWH has not been investigated. I hypothesize that PWH are vulnerable to amplified monocyte activation from exposure to the “second hit” of a sleep disorder. In Aims 1 and 2, I will utilize stored samples to evaluate monocyte activation in PWH by chronic and acute sleep exposure, respectively. Aims 1a and 1b will investigate if OSA and insufficient sleep are a) associated with a monocyte activation phenotype in PWH and b) explore if there is a differential effect of sleep disorder exposure on monocyte activation profiles by HIV status. In Aim 2, I will quantify the impact of acute sleep deprivation on monocyte activation among PWH who participated in an