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AIDS in Africa has potential to affect human evolution, UC Berkeley scientists report

Berkeley - If anyone doubts that epidemics can affect the course of human evolution, take a look at AIDS.

Three biologists from the University of California, Berkeley, show in this week's issue of Nature (May 31, 2001) that over a period of several generations, AIDS could alter the frequency of specific genetic mutations in African populations, delaying the average time between HIV infection and onset of disease.

Though this genetic evolution probably won't impact health management in Africa - public health experts pray that drugs or vaccines will soon cut the high mortality and infection rates on the continent - it provides a rare example of how epidemic infectious diseases can exert selective pressure on the human genome.

The only other widely accepted example of selection of this intensity caused by an infectious disease acting on a gene conferring resistance is malaria. Over hundreds of years, the disease selected for certain genes that increased the chance of human survival to reproductive age, but which caused other blood diseases, primarily sickle cell anemia but also the thalassemias.

"Natural selection in the case of AIDS in Africa is as strong as the selection malaria had on the gene that causes sickle cell anemia," said mathematical biologist Montgomery Slatkin, professor of integrative biology at UC Berkeley. "That's what surprised us."

Charles Darwin coined the term "natural selection" and focused on it as the driving force of evolution, whereby slight variations that increase the number of offspring tend to become more common in successive generations. The same idea is embodied in the phrase "survival of the fittest."

Scientists have speculated that infectious diseases that reached epidemic proportions over the course of history - from bubonic plague and measles to smallpox - have affected human evolution, selecting for genes that reduce mortality before or through the reproductive years. Evidence, however, is har
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Contact: Robert Sanders
rls@pa.urel.berkeley.edu
510-643-6998
University of California - Berkeley
29-May-2001


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