Generally, the telomeres in cells are sufficiently long that they can divide many times without a problem. Moreover, when fighting infections, T-cells can turn on an enzyme called telomerase, which can prevent the telomeres from shortening.
"The problem is that when we're dealing with a virus that can't be totally eliminated from the body, such as HIV, the T-cells fighting that virus can't keep their telomerase turned on forever," Effros said. "They turn off, and telomeres get shorter and they enter this stage of replicative senescence."
Previous studies have shown that injecting the telomerase gene into T-cells can keep the telomeres from shortening, enabling them to maintain their HIV-fighting function for much longer. This gene-therapy approach, however, is not a practical way to treat the millions of people living with HIV.
For the present study, rather than utilizing gene therapy, the researchers used a chemical called TAT2, which was originally identified from plants used in traditional Chinese therapy and which enhances telomerase activity in other cell types.
They tested TAT2 in several ways. First, they exposed the CD8 T-cells from HIV-infected persons to TAT2 to see if the chemical not only slowed the shortening of the telomeres but improved the cells' production of soluble factors called chemokines and cytokines, which had been previously shown to inhibit HIV replication. It did.
They then took blood samples from HIV-infected individuals and separated out the CD8 T-cells and the CD4 T-cells those infected with HIV. They treated the CD8 T-cells with TAT2 and combined them with the CD4 T-cells in the dish-and found that the treated CD8 cells inhibited production of HIV by the CD4 cells.
"The ability to enhance telomeras
|Contact: Enrique Rivero|
University of California - Los Angeles