SUNDAY, SEPTEMBER 25, 2016

Study examines neurological damage in HIV patients

Study results concerning neurological damage from HIV | Courtesy of sciencedaily.com
Researchers recently conducted a study to determine the reason why a significant number of HIV patients have neurological damage due to chronic inflammation stimulated by the patients’ immune system defenses.

"This type of approach allowed us to label macrophages in the perivascular space in the brain to identify macrophage and monocyte traffic to the brain in the early, mid and late stages of infection," Kenneth Williams, Boston College biology professor and the report's senior author, said. "We now know what cells bring the virus to the brain and what cells contribute to neurological damage in the brain, as well as the timing of the entry of these cells and when the pathologic virus enters. These are two big questions researchers have had." 

Despite the anti-retroviral drugs that seek to stifle symptoms, approximately half of individuals living with HIV still have neurological damage from chronic inflammation. Scientists have concentrated on macrophages and monocytes, which are disease-fighting cells in the immune system, to understand the roles of these cells in HIV-related neurological damage.

"An important question researchers have is what drives the pathology and the resulting damage in the brain?" Williams said. "Is it the virus itself or macrophage and monocyte cells? What we found is that these cells that arrive late with the development of AIDS have a 2.9-fold higher percentage of being infected with the virus. So there is a dramatic increase in the viral load as infection progresses that correlates to macrophage accumulation." 

The study, which involved Simian Immunodeficiency Virus-infected rhesus monkeys, allowed researchers to watch the disease-fighting cells accumulate throughout the brain during the infection’s different stages.

"Brain lesions are central to understanding what causes AIDS-related dementia," Williams said. "In early stages of infection, we could see two or three macrophages scattered along the vessel. By the late stage, when lesions appeared, there were 30 to 50 at the site. What we found is that a majority of the cells in the lesions were present in the brain at an early stage. So these macrophages are migrating from the brain to the lesion sites, which shows a complex and dynamic level of activity."