Combination antiretroviral therapy (cART) dramatically changed the face of the HIV/AIDS pandemic, making it one of the most prominent medical breakthroughs of the past 3 decades. However, as the life span of persons living with HIV (PLWH) continues to approach that of the general population, the same cannot be said regarding their quality of life.

CD4 dim CD8 bright T cells, a genuine population of CD8 + T cells, are highly activated and cytolytic. Recently, the low affinity IgG Fc fragment receptor CD32a was described as marker of HIV latency while others reported that CD32a is associated with T cell activation. Given that we have previously established that CD4 dim CD8 bright T cells are highly activated, mediate anti-HIV responses, and are infected by HIV, we assessed here CD32 expression on CD4 dim CD8 bright T cells in context of HIV. CD32 frequency on peripheral CD4 dim CD8 bright and CD4 + T cells was determined by flow cytometry among HIV negative and HIV positive patients. We report that among HIVindividuals, mean CD32 percent expression was 60% on CD4 dim CD8 bright T cells and 17% on CD4 + T cells (p<0.01). Among HIV + patients, mean CD32 percent expression was 54% on CD4 dim CD8 bright T cells and 12% on CD4 + T cells (p<0.001). CD32 expression on CD4 dim CD8 bright T cells did not correlate with CD4 count and viral load and was not different by HIV serostatus. CD32 was also higher on other double positive T cell populations in both HIV negative and HIV positive donors in comparison to their single positive T cell counterpart. Together, these studies indicate that CD32 is enriched on double positive T cells regardless of HIV serostatus. The functional role of CD32 on these double positive T cells remains to be elucidated.

HIV anti-retrovirals (ARVs) have vastly improved the life expectancy of people living with HIV (PLWH). However, toxic effects attributed to long-term ARV use also contribute to HIV-related co-morbidities such as heart disease, bone loss and HIV-associated neurocognitive disorders (HAND). Unfortunately, mouse models used to study the effects of ARVs on viral suppression, toxicity and HIV latency/tissue reservoirs have not been widely established. Here, we demonstrate an effective mouse model utilizing immune-compromised mice, reconstituted with infected human peripheral blood mononuclear cell (PBMCs). ARV is incorporated into mouse chow and administered daily. Combination ARV regimens included Atripla (efavirenz, tenofovir disoproxil fumarate, and emtricitabine) and Triumeq (abacavir, dolutegravir and lamivudine). Our model measures HIV-infected human cell trafficking, and ARV penetration throughout most relevant HIV organs and plasma, with a large amount of trafficking to the secondary lymphoid organs. Furthermore, te HIV viral load within each organ and the plasma was reduced in ARVs treated vs. untreated control. Overall, we have demonstrated a mouse model that is relatively easy and affordable to establish and utilize to study ARVs’ effect on various tissues, including the co-morbid conditions associated with PLWH, such as HAND, and other toxic effects.