Ingestion of the malaria pigment hemozoin renders human macrophages less permissive to HIV-1 infection

Juliette Diou, Sonia Gauthier, Mélanie R. Tardif, Rémi Fromentin, Robert Lodge, David J. Sullivan, Michel J. Tremblay

Research output: Contribution to journalArticle

Abstract

Few studies have investigated the pathophysiologic mechanisms responsible for what seems to be a possible interaction between Plasmodium falciparum, the causative agent of malaria, and HIV-1 in dually infected patients. It has been shown that Plasmodium parasites detoxify heme molecules into a pigment called hemozoin (HZ), which can significantly modulate the immune system. The primary objective of this study was to determine whether exposure of human primary monocyte-derived macrophages (MDMs) to the malaria pigment influences the process of HIV-1 infection. We report here that HIV-1 replication is significantly diminished in HZ-loaded MDMs. The HZ-mediated reduction in virus replication is due to a block at a step in the virus life cycle occurring between the completion of full-length reverse transcripts and integration of viral DNA within the host chromosome. Understanding the pathological mechanisms involved in P. falciparum and HIV-1 co-infection is of high importance because of possible therapeutic ramifications.

Original languageEnglish (US)
Pages (from-to)56-66
Number of pages11
JournalVirology
Volume395
Issue number1
DOIs
StatePublished - Dec 5 2009

Keywords

  • HIV
  • Hemozoin
  • Macrophage
  • Malaria

ASJC Scopus subject areas

  • Virology

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