People living with HIV face a greater risk of developing lung diseases at a much younger age, even if they have never smoked.
FIU researchers have now uncovered a previously unknown mechanism that helps explain how HIV causes emphysema and chronic obstructive pulmonary disease (COPD).
In a study published in Communications Biology, the team found that an HIV protein, known as Tat, essentially disrupts the lungs' internal molecular "clock" — the timekeeping system that regulates daily lung function and, importantly, plays a key role in immune response. This unleashes a cascade of chronic inflammation that damages airway tissue, setting the stage for disease.
"This is the first study to show HIV is interfering with this important system," said Hoshang Unwalla, lead study author and professor at the FIU Herbert Wertheim College of Medicine. "It opens the door for new ways to potentially slow or prevent disease development."
Unwalla has spent decades studying HIV's effects on the lungs. His lab was among the first to show that the virus can infect airway cells in the lungs and form reservoirs — pockets of HIV-infected cells that hide out and are not eradicated by antiretroviral therapies.
"When there are HIV reservoirs, the HIV-infected cells are still making these harmful proteins," Unwalla explained. "Tat, in particular, is the most damaging."
