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[Genetic Variation Increases HIV Risk In Africans (2008/07/16) on ScienceDaily]

The gene that the research focused on encodes a binding protein found on the surface of cells, called Duffy Antigen Receptor for Chemokines (DARC). The variation of this gene, which is common in people of African descent, means that they do not express DARC on red blood cells. DARC influences the levels of inflammatory and anti-HIV blood factors called chemokines.

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Discussing the findings, Professor Weiss said: "The big message here is that something that protected against malaria in the past is now leaving the host more susceptible to HIV.

"In sub-Saharan Africa, the vast majority of people do not express DARC on their red blood cells and previous research has shown that this variation seems to have evolved to protect against a particular form of malaria. However, this protective effect actually leaves those with the variation more susceptible to HIV."

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HIV affects 25 million people in sub-Saharan Africa today, an HIV burden greater than any other region of the world. Around 90 per cent of people in Africa carry the genetic variation, meaning that it may be responsible for an estimated 11 per cent of the HIV burden there. The authors observe that sexual behaviour and other social factors do not fully explain the large discrepancy in HIV prevalence in populations around the world, which is why genetic factors are a vital field of study.

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He W et al.:"Duffy antigen receptor for chemokines mediates trans-infection of HIV-1 from red blood cells to target cells and affects HIV-AIDS susceptibility.", Cell Host Microbe. 2008 Jul 17;4(1):52-62.

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[Malaria and HIV/AIDS interactions and implications (2004/06) on WHO]

HIV/AIDS and malaria are highly endemic, and there is wide geopgraphic overlap in sub-Saharan Africa. Among the most severely affected countries are Cameroon, Central African Republic, Malawi, Mozambique and Zambia where more than 90% of the population is exposed to malaria and HIV prevalence (among adults 15-49 years of age) is above 10%. Outside Africa, the two diseases overlap in certain at risk groups in South-East and South America, and in several Indian cities such as Mumbai.


HIV prevalence


Malaria

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[Geographic Spread of an AIDS-Resistant Mutation (2005/10/18O on PLoS]

Citation: (2005) Geographic Spread of an AIDS-Resistant Mutation. PLoS Biol 3(11): e397 doi:10.1371/journal.pbio.0030397


The discovery in the 1990s of a gene variant that thwarts HIV infection triggered development of a promising new class of medications. The gene normally encodes a protein receptor, called CCR5, that sits on the surface of white blood cells. HIV gains entry to these cells through CCR5. The variant gene, or allele, contains a mutation -- called ƒï¿½ï¿½32, because 32 base pairs are deleted -- that produces truncated CCR5 receptors that are useless to the virus, conferring resistance to individuals with both copies of the mutation, and delaying disease progression to those with one copy. The ƒï¿½ï¿½32 mutation also raised interesting questions for evolutionary biologists.

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About 10% of Europeans and inhabitants of western Asia carry the mutation, which researchers think evolved at least 700 years ago -- yet HIV emerged only about 50 years ago. According to population genetics theory, for a mutation to be neutral, or confer no selective advantage, it would have to be much older to occur at such a high frequency in the population. This inconsistency raised the possibility that the mutation spread because it provided an advantage against some other selective factor, now thought to be smallpox.

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This contour map shows the European distribution of the CCR5 ƒï¿½ï¿½32 variant, which was used to develop a method for studying the geographic spread of gene variants under positive selection