 We hypothesize that increased generation of activated factor X FXa contributes to a systemic elevation in pro-inflammatory cytokine levels e.g. IL-6 among HIV positive patients. This occurs, in part, via FXa activation of protease activated receptor 2 PAR-2 on monocytes and tissue macrophages, which perpetuates innate inflammation. We will test our hypothesis with an oral antagonist to FXa edoxaban, and quantify the immunologic effects of PAR-2 inhibition on systemic inflammation and monocyte activation. 