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.