The study will be published in the Nov. 15 print edition of the Journal of Immunology and is now available online.

Astragalus, also known as milk vetch, has long been used in traditional Chinese medicine, usually in combination with other herbs, to strengthen the immune system. It is still widely used in China to treat chronic hepatitis and as an adjunct therapy for cancer patients.

Astragalus has also been used to combat heart disease, as well as to prevent and treat common colds and upper respiratory infections.

The AIDS Institute study examined the relationship between TAT2, a chemical in Astragalus, and telomeres. Every chromosome has a telomere at its end that has a protective function -- similar to the plastic tip that keeps a shoelace from unraveling.

These telomeres get shorter every time a cell divides, and eventually the cell loses its ability to divide.

Immune cells must undergo a tremendous amount of division in order to effectively attack viruses that invade the body. Generally speaking, telomeres are long enough so that a great deal of cell division can take place without a problem. Moreover, when an infection is taking place, the CD8 T-cells -- the so-called killer T-cells -- can also activate telomerase, an enzyme that prevents the telomeres from shortening.

However, in the case of HIV, the virus can't be completely eradicated. The killer T-cells aren't capable of keeping the telomerase turned on indefinitely; at some point, it's switched off, the telomeres get shorter with every cell division, and the immune cells eventually lose their ability to fight the virus.

For the AIDS Institute study, the researchers exposed killer T-cells from HIV-infected persons to TAT2, the chemical found in Astragalus. They found that it not only slowed the shortening of the telomeres but also improved the cells' production of chemokines and cytokines, which had previously been shown to inhibit HIV replication.

They then took blood samples from HIV-infected individuals and separated out the killer T-cells (CD8 T-cells) from those infected with HIV (CD4 T-cells).

They treated the killer T-cells with TAT2 and then combined them with the HIV-infected T-cells and found that the treated killer T-cells curbed production of HIV.

In addition to fighting HIV, this strategy could be effective in combating other problems related to immunodeficiency, the researchers said, including the increased susceptibility to viral infections associated with chronic diseases or aging.