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

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.

• Authors: Juliette Diou, Sonia Gauthier, Mélanie R Tardif, Rémi Fromentin, Robert Lodge, David J Sullivan Jr, Michel J Tremblay
• Journal: Virology (Virology) Vol. 395 Issue 1 Pg. 56-66 (Dec 05 2009) ISSN: 1096-0341 [Electronic] United States
• PMID: 19801158 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Hemeproteins
• Pigments, Biological
• hemozoin

Topics

• Animals
• Cell Line
• HIV Infections (immunology, parasitology)
• HIV-1 (immunology, physiology)
• Hemeproteins (immunology)
• Humans
• Macrophages (immunology, virology)
• Malaria, Falciparum (immunology, virology)
• Mice
• Phagocytosis
• Pigments, Biological (immunology)
• Plasmodium falciparum (immunology)
• Virus Replication (immunology)