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Los Alamos National Laboratory Research Quarterly, Fall 2002
Stalking the AIDS Virus
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HIV and Natural Selection

Natural selection—Darwin's theory of evolutionary change—normally operates slowly, over decades, centuries, or millennia. Mutations occur in genes as a consequence of both environmental conditions and slightly error-prone processes that replicate DNA. Some of these mutations may be advantageous to an organism's survival and reproduction in the face of local environmental circumstances (the selective force). This genetic advantage results in preferential reproduction of the "fittest," which alters the makeup of the organism's local population, creating an altered or even a new species over time.

In the microbial world, the evolutionary process generally proceeds at a greatly accelerated pace, given the rapidity with which bacteria and viruses reproduce. Hence, in HIV infection, this evolutionary process occurs over the time span of months to years, rapidly altering the makeup of the viral population within a single individual. Viral mutations occur continually, the consequence of a massively error-prone RNA/DNA replication process. These viral mutants differ in the structure of the various proteins that mediate their exact form and function. The local selective environment is represented by the infected person's immune system—individualized by his or her HLA (and other) genetic makeup. It is that makeup that determines the ability of the person's antibodies and cytotoxic T cells to recognize and eliminate viral mutants.

But with HIV infections, so many new forms—so many viral mutants—arise that many cannot be eliminated. In a grim example of natural selection, the immune system "selects" those mutants that escape detection and elimination—favoring the survival of the fittest viral mutants at the expense of their human host. Each infected person thus accumulates a collection of "escape mutants" that differ from those of other infected individuals, an ironic outcome when we consider that the immune system generally protects us from succumbing to viral infections.

The research of Korber and others has supported the view that since an individual's HLA genetic makeup defines the viral mutants that he or she attacks—either vigorously, moderately, or weakly—that HLA supertype is a prime contributor to defining the population of escape mutants found in individuals. These surviving viral mutants are the "fittest" for aggressively infecting individuals with the same HLA supertype. They are less effective at infecting individuals with a different HLA supertype.

 

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