Like other kinds of cells, immune cells lose the ability to divide as they age because a part of their chromosomes known as a telomere becomes progressively shorter with cell division. As a result, the cell changes in many ways, and its disease fighting ability is compromised.
But the new study has shown that the chemical, TAT2, can prevent or slow this progressive telomere shortening.
"This has the potential to be either added to or possibly even replace the HAART (highly active antiretroviral therapy), which is not tolerated well by some patients and is also costly," said study co-author Rita Effros, a professor of pathology and laboratory medicine at the David Geffen School of Medicine at UCLA and member of the UCLA AIDS Institute.
The researchers 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 also improved the cells' production of soluble factors called chemokines and cytokines, which had been previously shown to inhibit HIV replication. And they found that 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 telomerase activity and antiviral functions of CD8 T-lymphocytes suggests that this strategy could be useful in treating HIV disease, as well as immunodeficiency and increased susceptibility to other viral infections associated with chronic diseases or aging," the researchers said
The study is to be published in the Nov. 15 print edition of the Journal of Immunology.