Description
We show that CECs originated from either the cord blood/placenta, peripheral blood of anemic and HIV patients mediate the exacerbation of HIV-1 replication in CD4+ T cells. Our observations coupled with RNAseq data demonstrate how interactions of CECs with CD4+ T cells via ROS affect the cell cycle machinery to facilitate HIV-1 replication. In addition, we demonstrate that CECs compared to mature RBCs express significantly higher levels of both CD35 and DARC, and can trans-infect HIV-1 to uninfected CD4+ T cells in vitro. Finally, our study indicates that HIV-1 interacts with CD235a on CECs and trans-infect uninfected CD4+ T cells in the presence of anti-retroviral drug, Tenofovir.