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Telomeres are specialized nucleoprotein structures capping ends of linear chromosomes, thus preventing the termini from being recognized as double-strand breaks. These structures are composed of repetitive sequences of guanine-rich hexameric DNA together with specific telomerebinding proteins. In addition to protecting of the chromosomes from damage and degradation, maintaining stable telomere complexes is indispensable for indefinite proliferation of specific cellular types, such as germ-line and cancer cells. The progress in our understanding of telomere biology indicates that manipulation of telomeres and telomerase could lead to clinically relevant applications in the diagnosis, prevention and treatment of cancer. Second reference and text: Aging means a decrease in vitality due to age, subjectivity to various diseases. This is a universal situation, which is the same for all organisms, only at individual speeds. From the molecular point of view, it is an inability to renew the correct structure of biomolecules for an unlimited time = „systemic molecular disorder“ (Hayflick). Telomere is an end section of the chromosomal DNA, consisting of many times repeated short sequence, to which specific proteins binds. You can imagine telomeres such as “caps”, which are placed on both ends of each chromosome and protect them against damage (e.g. by a transfer of part of chromosomes to another – the so-called nonreciprocal – e.g. by a transfer of one chromosome to another – the so-called translocation). During each cell division, telomeres are shortened a little and when they reach a certain critical value, chromosomes are damaged and the cell division stops or cells die. P Telomerase prevents shortening of telomeres and thereby facilitates cell Davison. The ability of a cell to divide decreases with age. The reasons are DNA structures, marked as telomeres, which protect the ends of chromosomes and which are shortened a little during each cell division. When almost nothing is left, the cell stops dividing and then it dies. Division is important especially for immune system cells, which use division to respond to the presence of an infection. The number of their possible divisions, unlike most other body cells, is increased by the enzyme telomerase, which prevents shortening of telomeres. However, the enzyme telomerase in patients infected by HIV does not prevent shortening of telomeres. In patients infected by the HIV virus, scientists have found many dysfunctional T-lymphocytes with short telomeres, which indicates that working of their enzyme telomerase has its limits. Previous studies showed that shortening of telomeres can be prevented by means of the gene therapy, when genes for telomerase are inserted into T lymphocytes. Such modified bubbles can then war with the HIV virus for a much longer time. The problem is that this approach cannot be used to treat millions infected people and experts are looking for alternatives. One of them is described by scientists from the California University in Los Angeles in the expert magazine Journal of Immunology. They found out that a substance isolated from the plant Astragalus membranaceus has similar effects on T lymphocytes as gene therapy. The plant Astragalus (), which is abundantly used in the traditional Chinese medicine. The compound called TAT2 works as an efficient activator of telomerase, which slows down shortening of telomeres. Moreover, it increases the ability of cells to produce soluble factors cytokines and chemokines, which are crucial for some patients, in order that their immune system works again. Their very production is usually decreased in cells of patients infected by the HIV virus. The study authors also claim that TAT2 sis a great addition, where in some cases even potential replacement of combined antiviral therapy is considered (HAART),which could prolong the life of people affected by the HIV virus. Source: Telomerase-Based Pharmacologic Enhancement of Antiviral Function of Human CD8+ T Lymphocytes, , Steven Russell Fauce,, Beth D. Jamieson†, Allison C. Chin , Ronald T. Mitsuyasu, Stan T. Parish, Hwee L. Ng, Christina M. Ramirez Kitchen, Otto O. Yang, Calvin B. Harley and Rita B. Effros.