HIV is known to grind the immune system. But exactly how his main goal - a class of immune cells called CD4 T-cells - is driven to extinction has been debated vehemently. One side argues that HIV kills cells and depletes an immune system that is desperately make replacements. The other side believes that the virus stifles line power CD4 cells. Now, results of a new technique, reported in the January issue of Nature Medicine , lend support to the idea that HIV interferes with the production of T cells
For deal with this thorny issue, a team led by immunologist Joseph McCune of the University of California (UC), San Francisco, and endocrinologist Marc Hellerstein UC Berkeley used an innovative method ( science , the February 20, 1998, p. 1133). They infused intravenously subjects with a glucose solution - a precursor of deoxyribose, one of the chemical building blocks of DNA - in which glucose molecules containing deuterium, a non-radioactive isotope of hydrogen. They then took blood samples at different times after the infusion was completed. As T cells divided, the DNA of deuterium-labeled was gradually replaced by unlabeled DNA, allowing the team to calculate the rate of new cells and their average lifetime production.
On average, the T cells had shorter lifetimes in patients infected with HIV untreated than in uninfected controls, suggesting that the virus was killing them. But the T-cell levels in patients infected production was higher than in controls, as expected if the immune system has worked overtime to replace the destroyed cells. And patients taking antiviral drugs that have drastically reduced their HIV rates have higher T-cell production levels that control and untreated groups - the opposite of what would be expected if increased production were all simply a response to the destruction of T cells by HIV. Instead, the authors suggest, antiviral therapy led to a "disinhibition" of production machinery.
For some researchers, the new document essentially solves the controversy. In an accompanying article in Nature Medicine immunologist Giuseppe Pantaleo of Vaudois Hospital Center in Lausanne, Switzerland, summarily states that the study "puts an end to four years of excitation (often rude) debate" on the problem. But supporters of the model of "immune exhaustion" argue that non-HIV patients can still deplete their immune system, which should replenish their smaller pool of immune cells much more quickly than uninfected people do.
McCune said that if HIV is in fact interfere with the production of new T cells, the findings could point to new strategies to improve production. For example, T cells can be cultured outside the body for subsequent reintroduction of the disease, or patients can receive molecules called cytokines to induce immune cells to divide signaling.
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