Every cell contains a tiny cellular clock called a telomere, which shortens each time the cell splits in two. Located at the end of the cell's chromosome, the telomere limits the number of times a cell can divide.
"Immune cells that fight HIV are under constant strain to divide in order to continue performing their protective functions. This massive amount of division shortens these cells' telomeres prematurely," explained Dr. Rita Effros, Plott Chair in Gerontology and professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA. "So the telomeres of a 40-year-old person infected with HIV resemble those of a healthy 90-year-old person."
Most scientists agree that telomeres evolved to avert the rampant cell growth that often leads to cancer. Yet many cancers continue growing because they undergo genetic changes and start to produce telomerase, which regenerates their cells' telomeres.
Effros and first author Mirabelle Dagarag, Ph.D., hypothesized that harnessing telomerase's power over telomeres may provide a potent weapon in helping the AIDS patient's exhausted immune system defend itself against HIV. The researchers extracted immune cells from the blood of HIV-infected persons and tested what would happen if telomerase remained permanently switched on in the cell.
"By exploiting telomerase's growth influence on telomeres, we thought we might be able to keep the immune cells youthful and active as they replicated under attack," said Dagarag, a postgraduate researcher. "We used gene therapy to boost the immune cell's telomera
Contact: Elaine Schmidt
University of California - Los Angeles