HIV-Tat Induced Differential Regulation of SCARB1 and MSR1 in Human Microglial Cells

Microglia are the resident immune cells of the central nervous system (CNS), involved in clearing debris, regulating inflammation, and maintaining neuronal health. Surface receptors, including SCARB1, MSR1, and CD36, tightly regulate their function. In HIV-associated neurocognitive disorders (HAND), chronic exposure to viral proteins such as HIV-Tat disrupts microglial homeostasis, potentially exacerbating neuroinflammation and neurodegeneration. 1 In this study, we investigated the baseline expression of SCARB1, MSR1, and CD36 in human microglial (HMC-3) cells and evaluated the temporal effect of HIV-Tat (50 ng/mL) exposure at 24 and 48 hours. Heat-inactivated Tat (HI-Tat) and untreated cells served as controls. RT-PCR was used to assess gene expression, followed by densitometry analysis. We observed that SCARB1 was the most abundantly expressed receptor at baseline, followed by MSR1 and CD36. Upon HIV-Tat exposure, SCARB1 was significantly elevated at 24 hours but declined by 48 hours. In contrast, MSR1 expression appeared reduced at 24 hours but was significantly upregulated at 48 hours. These results suggest a time-dependent modulation of scavenger receptors by HIV-Tat, which may contribute to altered microglial activity and chronic neuroinflammation in HAND.