The astragalus root has recently been discovered as a major breakthrough as an alternative treatment in HIV/AIDS patients, as noted by researchers at the UCLA AIDs Institute. It offers both a natural and cost effective method to treat this disease. Many patients have limited results when being treated with HIV/AIDS drugs and these drugs can be very expensive.

In Asia, the Chinese use the astragalus root in the treatment of heart disease, diarrhea, and the immune system. As cells age, they lose their ability to divide and lose their disease fighting capabilities. Thus, the immune system is compromised. The astragalus root has shown success in curbing the development of telomere, which is the area in the rear of each chromosome cell, and it contains the repeated DNA series without genes; hence the telomeres instead protect the chromosome ends from becoming fused as one.
Of the 50 most utilized herbs in ancient Chinese remedies, astragalus is the most prolifically used of any of them. It is usually boiled in water or the roots used in soups and it has properties proven to improve human immunity to disease, so much so that it has raised the hopes of many researchers worldwide. There is optimism in the ranks of HIV research because of the capacity to augment telomerase action as well as the antivirus utility of CD8T-lymphocytes that leads researchers to believe a useful stratagem for treating HIV virus could be in expected or perhaps likely in the future.

Cell aging reduces the capability of cell division due to the telomere portion of the chromosome reducing regularly during cell separation. The consequence of this is the many variations of divided cells and the immunity potential then becomes suspect and even negated. When the cell can’t divide any longer this is known as replicative senescence and may appear that the cell has reached its end, though this is not the case, since the cell has simply morphed into a cell with fresh genetic and well-designed uniqueness.

Massive amounts of cell separation is required in the immunity system for this human immune structure to complete its role correctly. For instance, the aptly named “killer” CD8 T cells, which battle against infection, have exclusively sensitive nerve endings for exacting antigen matches. When a body is invaded by virus, those killer T cells, whose receptors distinguish that the virus, by virtue of its dividing, has created versions of itself, which now also enter into immunity combat against the viral invader.

Usually the telomeres within the cells are indeed lengthy enough that their ability to divide over and over again without trouble is not compromised. While fighting infections, T cells may introduce the telomerase enzyme thereby stopping any shortening of the telomeres. A large obstacle in this HIV fight or any virus is the T cells do not have the ability to produce telomerase indefinitely. The T cells will shut off, telomeres shorten and they enter into the replicative senescence phase.

Earlier testing has revealed when injection of the telomerase gene into T cells takes place, this may keep the telomeres from getting shorter thus allowing them to continue their battle against the HIV virus for a longer period. As a genetic therapy method, this really is not the most realistic method of treatment for the tens of millions of HIV sufferers worldwide.

In the most current study, instead of using genetic therapy, scientists utilized a compound known as TAT2 that had its origin from the astragalus plants that are widely used in traditional Chinese medicine and are known to activate telomerase actions in cells when tested. Tests were conducted in a few ways with TAT2. Initially showing the CD8 T cells from an HIV positive individual to TAT2 to measure if the compound actually stymied the shortening of telomeres and if the cells manufacture improved of soluble factors referred to as chemokines and cytokines which had already shown the ability to hinder HIV replication and it did!

Researchers then gathered blood samples of HIV infected patients, separating the CD8 T cells along with CD4 T cells that are the ones infected with HIV. They then treated the CD8 T cells with their TAT2 then mixed them among the CD4 T cells in the lab dish and realized their treated CD8 cells actually inhibited the manufacture of HIV via the CD4 cells.

This capability to improve telomerase action as well as the antiviral utility of the CD8 T – lymphocytes puts forward that this stratagem has the potential to be used in the treatment of HIV illness and the immunodeficiency plus the amplified vulnerability to more viruses out there that are linked with persistent illness or simply aging.

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