Our genes are amazing. They win battles for us against some pathogens (malaria), but their victories can leave us exposed to others (HIV). That’s the lesson from a fascinating paper published recently in Cell and Host Microbe.
Researchers looking at data from a large group of American servicemen have found that a genetic mutation which made people of African descent less susceptible to a now-extinct form of malaria also makes them more likely to contract HIV. That’s the bad news. The good news is that African-Americans with the mutation survive longer with HIV if they do get infected.
The paper is very dense, full of sentences like this:
“As there is extensive linkage desequilibrium around the DARC locus, we cannot exclude with certainty the possibility that the effects ascribed to the -46C/C genotype might be attributable to some other polymorphism(s)/genes in the LD near DARC”
But it’s been magicked into comprehensibility by Nicholas Wade, writing in the New York Times. Wade’s account of the research, a model of clear science writing, translates the DARCS and -46C/Cs into passages like this:
“The Texas-London research team is not certain how lack of the receptor promotes H.I.V. infection, but Dr. Ahuja said the red blood cells acted like a sponge for CCL5. Because CCL5 is known to obstruct multiplication of the virus, having lots of the hormone in the bloodstream may prevent infection. Conversely, people whose blood cannot soak up the hormone could be more vulnerable.”
While the people whose blood contributed to the study were all Americans, the paper suggests that the genetic modification is likely to occur also in the African populations with whom the African-Americans share ancestors. And it may explain some of the high HIV prevalence in sub-Saharan Africa. Of course HIV is distributed unevenly throughout the continent and even within particular countries; it would be interesting to map the distribution of the genetic variation.