Malaria hemozoin modulates susceptibility of immature monocyte-derived dendritic cells to HIV-1 infection by inducing a mature-like phenotype.
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.
Diou
Juliette
J
Centre de Recherche en Infectiologie, Université Laval, Québec, Canada.
Tardif
Mélanie R
MR
Barat
Corinne
C
Tremblay
Michel J
MJ
D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000821:virology; D002460:Cell Line; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000469:parasitology / Q000821:virology*; D015536:Down-Regulation; D015497:HIV-1 / Q000254:growth & development*; D006420:Hemeproteins / Q000502:physiology*; D006801:Humans; D009000:Monocytes / Q000469:parasitology / Q000821:virology*; D010963:Plasmodium falciparum / Q000472:pathogenicity*; D019713:Receptors, CCR5 / Q000096:biosynthesis; D015728:Receptors, HIV / Q000096:biosynthesis; D037521:Virulence Factors / Q000502:physiology*
D006420:Hemeproteins; D019713:Receptors, CCR5; D015728:Receptors, HIV; D037521:Virulence Factors; C020753:hemozoin