From The New York Times:

A genetic variation that once protected people in sub-Saharan Africa from a now extinct form of malaria may have left them somewhat more vulnerable to infection by H.I.V., the virus that causes AIDS. The gene could account for 11 percent of the caseload in Africa, explaining why the disease is more common there than expected, researchers based in Texas and London say.

The eleven percent figure is interesting -- not quite sure how they came up with that. But it would make sense that a vulnerability of this kind would account for some of the radical disparity in HIV infections in Africa versus other continents.

The variation historically protected against a previous strain of malaria -- not the strain most common today:

The genetic variation, called a SNP (“snip”), involves a change in a single unit of DNA. This particular snip has a far-reaching consequence, that of preventing red blood cells from inserting a certain protein on their surface. The protein is called a receptor because it receives signals from a hormone known as CCL5, which is part of the immune system’s regulatory system.

The receptor is also used by a malarial parasite called Plasmodium vivax to gain entry to the red blood cells it feeds on. Some 10,000 years ago, people in Africa who possessed the SNP gained a powerful survival advantage from not being vulnerable to the ancestor of Plasmodium vivax. The SNP eventually swept through the population and the vivax parasite died out in Africa, to be replaced by its current successor, Plasmodium falciparum.

More than 90 percent of people in Africa now lack the receptor on their red blood cells, as do some 60 percent of African-Americans.

What are the implications here for the disparities in new infections among African-Americans in the United States -- particularly given the data that shows that Af-Am's do not engage in more "risky" sex than their white counterparts? More research is needed here!