In the setting of HIV infection, the effect of an unfavorable genetic background was similar to traditional CAD risk factors and certain adverse antiretroviral exposures. Genetic testing may provide prognostic information complementary to family history of CAD.

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Purpose of Review There is increasing evidence pointing towards an important role of heightened immune activation and inflammation in PLWH contributing to the development of non-AIDS co-morbidities. This review aims to explore low BMD in HIV with a focus on the underlying mechanisms and relationships between the immune and skeletal systems. Recent Findings Baseline immune activation and inflammation negatively impact BMD at ART initiation. B- and T-cell alterations in HIV lead to an imbalance in the osteoblastic (OPG) and osteoclastic (RANKL) cytokines which favours osteoclastogenesis and bone resorption. These findings suggest an important role for immune mediated mechanisms in the pathogenesis of low BMD in HIV. Summary Bone homeostasis is in part regulated by cells of the immune system through complex interactions with the RANK/RANKL/OPG axis. Disturbances in the normal functioning of T-, B-cells and monocytes in HIV and the resulting pro-inflammatory state may contribute to dysregulation of this finely controlled balance leading to increased bone loss. Pre-ART levels of immune activation and inflammation have a consistently negative effect on BMD and further suggests the immunocentric basis of bone loss in HIV alongside supporting the benefits of earlier ART initiation. Further longitudinal studies will help determine the effect this will have on fracture risk in PLWH.