December 11, 2000

BIRMINGHAM, AL — A new study by researchers at the University of Alabama at Birmingham (UAB) provides new information about how HIV-associated dementia develops in patients infected with HIV. An article detailing the findings was published in the October 2000 issue of the Journal of Virology by lead investigators Olaf Kutsch, Ph.D., a post doctoral fellow in cell biology at UAB, and Etty Benveniste, Ph.D., professor and chair of cell biology at UAB.

“We discovered that HIV Tat, a molecule secreted by infected HIV cells, is responsible for the production of proteins in the brain that attract harmful immune cells,” Benveniste says. “It is the invasion of these immune cells into the brain that leads to HIV dementia, a degenerative brain disease characterized by loss of cognitive abilities and behavioral and motor impairments.”

Proteins called chemokines act as homing devices, attracting immune cells to the brain. “We knew that these chemokines are produced by certain cells in the brain,” Benveniste says. “Our study showed that HIV Tat is one of the molecules responsible for activating the cells to produce these chemokines.”

HIV Tat is introduced into the brain by HIV-infected cells that have penetrated the brain’s protective barrier. “In patients with HIV-associated dementia and other patients with neurological diseases, the protective barrier is broken, allowing immune cells into the brain,” Benveniste says. “The consequence is detrimental. In patients with HIV, infected immune cells traffic through the barrier and subsequently infect cells in the brain, leading to cellular dysfunction.”

The study suggests that by controlling the production of chemokines in the brain, it may be possible to prevent or reduce the risk of HIV-associated dementia in patients infected with the virus. “That is why more research must be done to identify the sources and stimulators of chemokine production in the brain,” Benveniste says.