"Long before it's in the papers"
June 04, 2013


AIDS deadliness might be evolutionary accident, researchers find

June 15, 2006
Courtesy Cell Press
and World Science staff

AIDS would be a much milder condition, researchers say, were it not for an evolutionary accident that made the virus behind the disease much more virulent.

The illness has killed more than 25 million people since it was recognized in 1981, according to the Joint United Nations Programme on HIV and AIDS. Last year an estimated 4.1 million were newly infected.

Many monkeys have a virus called simian immunodeficiency virus, or SIV, believed to be ancestral to the one behind AIDS. But the primates seldom suffer the symptoms associated with the human form of the disease.

It turns out that monkey forms of the virus contain a molecule that helps it evade the immune system, the scientists said. Paradoxically, they added, this molecule also protects the immune system from the pathogen. 

The molecule, a protein called Nef, reduces the activity of immune system cells called T cells, the researchers argued. This keeps the immune system from going into an overdrive mode that is damaging to itself.

Most members of this viral family have Nef, said the researchers. But tragically, the protein lost its protective function at some point in evolution, in certain variants of the virus. Present-day HIV-1, the virus responsible for human AIDS, lacks the property, the scientists reported.

Nef may “explain why many monkey species naturally infected with SIV do not develop disease,” said Frank Kirchhoff of the University of Ulm in Germany, one of the researchers. Researchers have known of the protein for some time, he added, but assumed it was a “bad guy”; the new research suggests a more complex picture. 

A few strains of the monkey forms of virus also lack Nef, he added, with similar deadly effects. “The findings suggest that the gene function was lost during viral evolution in a lineage that gave rise to HIV-1,” the researchers said in a statement. The findings appear in the June 16 issue of the research journal Cell.

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