Study Suggests Macrophages As Focus Of New HIV Drug Development
According to a study recently published on the PLoS One Web site, immune cells called macrophages may be an important target for new HIV-related drug development. The authors of the study verified that HIV-infected macrophages are responsible for damaging tissues and serve as reservoirs for the virus during treatment.
Researchers investigated 780 HIV genetic sequences from 53 abnormal and normal tissue samples. The samples were collected post mortem from seven patients who died from AIDS-related diseases between 1995 and 2003. Samples from lymphoid tissues (HIV associated with macrophages and T-cells), and non-lymphoid tissues (HIV restricted to macrophages) were compared to assess the presence of recombination within the infected individual.
Recombination occurs when pieces of genetic information from several HIV viruses combine to form a new mutant strain. HIV treatments cannot recognize these new mutant strains, thus allowing the virus to continue multiplying within the body.
Researchers ultimately found that up to 50 percent of the sequences studied from abnormal lymphoid tissues and macrophage-rich non-lymphoid tissues were recombinant sequences. The presence of recombination, especially in macrophage associated HIV tissues (non-lymphoid tissues), suggests that macrophages play a large role in HIV replication.
Moreover, a greater frequency of recombinant sequences was found in diseased (abnormal) tissues. This is a result of the inflammatory response, which causes increased macrophage production. The inflammatory response is the body’s reaction to any disease or injury, which triggers the immune system to send cells and chemicals (in this case, macrophages) to the infected site.
The study implied that without targeting macrophages through drug therapy, eliminating HIV-1 may be impossible, as macrophages will serve as sites for extensive HIV recombination and thus evolution of the virus.
For further details, see the research article at the PLoS One Web site.
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