This depletion is an effect of HIV infection, since it was not observed in the HIV-negative population and probably involves the particular role of the HIV-Tat protein’s enhancement of vascular adhesion and trans-endothelial migration of monocytes reported by other investigators.20 HIV-infected monocytes are known to migrate more efficiently across vessel walls, while maintaining their infectivity.8 We conclude that the Lub blood group contributes to the depletion of circulating phagocytes, possibly by enhancing their margination and extravasation.2 The gene discussed is TAT; the disease is HIV infectious disease.