Although people with HIV now live substantially longer than they once did, they also suffer inordinately from other chronic diseases. EVMS scientists have received funding from the American Heart Association to study one of the deadliest culprits — atherosclerosis.

“Atherosclerosis (a buildup of plaque within the arteries) is one of the leading causes of mortality among HIV+ people,” says Elena Galkina, PhD, Professor of Microbiology and Molecular Cell Biology, principal investigator for the $200,000, two-year grant from the American Heart Association’s Innovative Project Award program.

Joining Dr. Galkina in her research are co-investigator Ming-Lei Guo, PhD, Associate Professor of Pathology and Anatomy, and consultant Larry Sanford, PhD, Professor of Pathology and Anatomy.

“Evidence suggests that the body’s immune response might be involved in accelerating HIV-associated atherosclerosis development,” says Dr. Galkina, who along with her collaborators is a member of the EVMS Center for Integrative Neuroscience and Inflammatory Disease.

While medications have proven highly successful in suppressing HIV, scientists know that reservoirs of the virus remain hidden within the brain.

“Virtually nothing is known about the effects of HIV-associated neuroinflammation on atherogenesis and the immune response accompanying this pathology,” Dr. Galkina says.

During the research, Dr. Galkina and her colleagues will focus on the “regulatory protein” Trans-Activator of Transcription (TAT), which is expressed upon HIV infection and is involved in HIV-related medical issues. The importance of TAT expression in brain pathology has been shown, Dr. Galkina says, but the role of TAT-induced neuroinflammation in shaping immunity and atherosclerosis development is unclear.

The scientists will determine to what extent brain-associated TAT expression alters the immune response and accelerates atherosclerosis. They also will examine how neuroinflammation impacts the amygdala, an almond-shaped structure within the brain. They believe that the amygdala — compromised by the inflammatory immune response — may be key to supporting the development of atherosclerosis.

“The major innovation is the overall concept that TAT-induced neuroinflammation alters brain functions, resulting in activated peripheral immune response and atherogenesis,” Dr. Galkina says.

The research dovetails with the AHA mission of developing innovative research models in the areas of cardiovascular research, and expanding multidisciplinary collaborations that would open new avenues for the development of new therapeutics for cardiovascular disease.