Among HIV patients, as many as 69.4 percent are afflicted with peripheral neuropathy of the arms, legs, hands, feet, fingers and toes. The most common neurological disorder associated with people living with HIV, it is known as "dying back", a painful condition where sensory nerves die and then retreat, causing a loss of sensitivity and function.
Burdo, an associate research professor in the lab of Professor of Biology Ken Williams, said the group has been exploring the connection between peripheral neuropathy and inflammation in the dorsal root ganglia located outside of the spine. The focal point is macrophage activation, the disruptive activity of cells associated with the body's immunological response to infection.
The presence and behavior of those cells could help to determine what triggers peripheral neuropathy in HIV patients, Burdo said.
"We're studying what's going on in dorsal root ganglia in terms of inflammation by macrophage activation and correlating that to this nerve loss," said Burdo.
Central to the study, funded by the NIH's National Institute of Neurological Disorders and Stroke (NINDS), is the molecule CD163, identified by Burdo and Williams as a biological marker for the activation of macrophages and monocytes in patients with HIV.
Burdo said the team hopes to develop a clearer understanding of the progression of peripheral neuropathy, how to pinpoint early and advanced stages of neuropathy with biomarkers, and potential drug therapies that could stop or slow the disease.
Provided by Boston College
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