Voila pour la petite histoire.

Dr. Weiss said the red blood cell receptor was similar to another receptor, CCR5, which occurs on the surface of the white blood cells that are H.I.V.’s major target. A small percentage of Europeans have a mutation that prevents the CCR5 receptor from being displayed on the surface of white blood cells, and they are protected against H.I.V.

It is somewhat puzzling that the absence of the two receptors has the opposite effect — vulnerability to H.I.V. when the red cell receptor is missing, protection from it when the white cell receptor is withdrawn. The researchers offer an explanation that they concede is far from straightforward.

“If you found the paper plain sailing, most of my students didn’t,” Dr. Weiss said. As is often the case with provocative new findings, the researchers may have some way to go before convincing others that their observation is correct. Dr. Goldstein said that in parts of the United States, African-Americans have a higher infection rate than European-Americans, and that patients with a higher proportion of African genes may be more vulnerable to H.I.V. for reasons unconnected to the SNP. Nonetheless, the SNP would show up in a greater proportion of infected people simply because of their African heritage. If so, the gene’s apparent association with H.I.V. infection could be just coincidental, not causal.

Source : The New York Times.