Abstract Phagocytosis is a critical component of the immune response to viral infection, resulting in the clearance of infected cells, while minimizing exposure of uninfected cells. HIV is able to evade this response through suppression of key regulators of phagocytosis. Programmed death 1- homologue (PD-1H) has been identified as a co-inhibitory molecule that suppresses activation of T cells during infection and cancer immunogenesis. However, our evidence indicates that PD-1H may also play a significant role during immune response to HIV infection via upregulation and subsequent phagocytosis of infected T cells. HIV-induced apoptosis and monocytic cell engulfment was tested utilizing CEMSS T cells as target cells and monocyte derived macrophages (THP-1), as phagocytic cells. Cells were infected with a GFP-labeled HIV strain, NL4-3. HIV-infected T cells displayed greater apoptotic activity (approximately 9.0%) relative to mock-infected controls. Concurrently, phagocytosis of HIV-infected T cells increased approximately 4-fold. Expression of PD-1H on infected T-cells was detected on 16.7% of cells, which correlated with increased phagocytosis. When an antagonistic antibody against PD-1H was used, the number of phagocytic cells was reduced by a factor 2, which was replicated utilizing human stem cell derived dendritic cells. Phagocytosis was also confirmed by the upregulation of IL-1β, which was 5 fold higher relative to controls. Here we demonstrate that PD-1H facilitates monocytes-derived macrophages or DCs to phagocytize HIV-infected T cells in cell based assays. Based on these results we believe that further study in humanized mouse models of HIV infection is warranted.