November 17, 2008
Telomeres are protective regions at the end of the cells' chromosomes, which shorten each time a cell divides. When telomeres become sufficiently short, cells reach a stage known as replicative senescence in which they can no longer divide.
The enzyme known as telomerase prevents telomeres from shortening when activated. Unlike most of the body's cells, immune system cells upregulate telomerase with their activation. However, with aging or chronic infection with HIV, there is an increase in the proportion of dysfunctional CD8 T-cells with short telomeres, demonstrating that telomerase has a limited effect.
"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," explained UCLA AIDS Institute member Rita Effros. "They turn off, and telomeres get shorter and they enter this stage of replicative senescence."
In a study described in the November 15, 2008 issue of the Journal of Immunology, Dr Effros and her colleagues tested a compound known as TAT2, originally derived from the Chinese herb astragalus, on CD8 T-cells from HIV-infected individuals. They found that TAT2 retarded the shortening of the cells' telomeres as well as improved their production of chemokines and cytokines that help inhibit HIV replication.
"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 authors write.
Dr Effros added, "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."
—D Dye
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