Malaria hemozoin modulates susceptibility of immature monocyte-derived dendritic cells to HIV-1 infection by inducing a mature-like phenotype

P>Together, Plasmodium falciparum (P. falciparum) and HIV-1 infections cause more than four million deaths a year. There is still limited information about the putative impact of the malaria pigment hemozoin (HZ) on the dissemination of HIV-1. As so, we propose a premise where HZ present in human dendritic cells (DCs) could modulate HIV-1 transfer to CD4+ T cells. We report here that HZ promotes transmission of HIV-1 by immature monocyte-derived DCs (iMDDCs). Moreover, we noted that in the presence of HZ, iMDDCs were less permissive to productive HIV-1 infection. The HZ-dependent modulation of the interaction between iMDDCs and HIV-1 seems to be partly due to a decreased expression of CCR5 and also to the induction of a more mature phenotype as proven by microscopy and flow cytometry analyses. Therefore, exposure of iMDDCs to malaria pigments provokes their maturation rendering them more potent to trans-infect CD4+ T cells with HIV-1.