Abstract
Renal biopsy data suggest that renal tubular cells may serve as a reservoir for HIV-1, however the mechanism underlying this finding has not been studied. Here we show that primary human renal proximal tubular epithelial cells (HRPTECs) have the potential to harbor HIV-1 through the DEC-205 receptor. The interaction of HIV-1 with DEC-205 results in the rapid internalization of the virus for lysosomal degradation, without establishing a productive infection. However, a small fraction of incoming virus escapes degradation and can be rescued by T cells. Since pH-modulating agents and an inhibitor of endosomal transport increased HIV-1 accumulation and trans-infection to T cells, it appears that HRPTECs endocytic compartments may be the site of viral persistence and transmission to target cells. The ability of T cells to rescue the virus from HRPTECs further supports the hypothesis that these cells have the potential to serve as a reservoir for HIV-1.