HIV-associated brain damage occurs extensively, even in patients who are taking otherwise effective traditional anti-HIV therapy. This is a result of potent cooperation between two types of special immunological cells within the brain called monocytes and platelets. A recent paper published by University researchers in the Journal of Immunology demonstrates the presence of these platelet-monocyte ‘teams’ in HIV infected individuals and how these teams lead to increased neuronal damage.
HIV infection in the brain often results in major inflammatory responses and massive loss of critical neurons. HIV is known to enter the brain via infected monocytes, which have to cross a specialized barrier known as the blood brain barrier to infect brain cells. Crossing the brain barrier is not an easy step, and monocytes can cross only when they are exposed to inflammatory mediators secreted by platelets or when they come in close contact with platelets, forming platelet–monocyte complexes.
Researchers found that during HIV infection, platelets get ‘turned on’ and they interact more frequently with monocytes. These platelet-monocyte duos promote inflammation and cause an increase in the migration of monocytes across the blood brain barrier. The authors demonstrate that HIV infected individuals exhibit increased levels of platelet-monocyte complexes as compared with uninfected individuals.
The research team, led by Sanjay B. Maggirwar, M.B.A., Ph.D., Professor in the Department of Microbiology and Immunology at the School of Medicine and Dentistry, used brain specimens collected from HIV infected patients. Despite successful therapy, HIV-1 infected individuals participating in the study showed the presence of neuronal damage due to the increased circulating platelet-monocyte complexes within their brain.
This finding stresses the need to promote novel therapies that would supplement traditional anti-HIV therapy and help in preventing the neurological problems often seen in individuals with HIV. The findings outlined here suggest that targeting platelet activation or thwarting the formation of platelet-monocyte complexes could be novel interventions in combating HIV related brain damage.