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Los Alamos National Laboratory Research Quarterly, Fall 2002
Stalking the AIDS Virus
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How HIV Cripples

T-helper cells function as the central processing unit of the immune system. They respond to invading pathogens by releasing signals (cytokines) that regulate a broad spectrum of immunological functions, such as antibody production, inflammation, the activity of scavenger white blood cells, and even the production of new red blood cells. Because of its molecular structure, HIV can infect all T-helper cells, and infected T-helpers thus become reservoirs for replicating the virus—vehicles for its spread to millions of other T-helpers. As the virus spreads through the bloodstream, antibodies—which are effective only outside cells—can shield additional T-helpers from becoming infected. Unfortunately, HIV evolves so rapidly within a single individual that it evades the antibody responses that would protect new cells from infection. This cycle of antibody production and HIV escape occurs repeatedly over the course of an infection. In addition, HIV can also be passed directly from infected to uninfected T-helpers, thereby completely bypassing the protective shield of antibodies.

Therefore, controlling HIV infection requires eliminating the infected T-helper cells. This is the purview of cytotoxic T cells (CTLs), which recognize infected T-helpers by "seeing" small pieces of viral molecules (epitopes) presented by HLA-A, -B, and -C proteins on the infected T-helper's surface. CTLs kill infected cells in most viral infections, but usually the cells that they kill are expendable—replaced by the cell division of still-healthy cells (for example, cells lining the digestive system). Unfortunately, in the case of HIV infection, the T-helper cells that are killed are crucial to the immune system's regulation, and, therefore, the actions of the CTLs have serious consequences. Ultimately, the combination of HIV-induced and CTL-induced cell death is not compensated by the production of new T-helpers, and over a period of years, this imbalance reduces the number of T-helpers enough to compromise the immune system's ability to respond to other infections. At this point, symptoms of AIDS ensue, with patients commonly succumbing to the secondary infections; hence, the viral nomenclature—human immunodeficiency virus.

 

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