The mutation that protects against HIV would have appeared under the pressure of epidemics "hemorrhagic fever

Repeated outbreaks of "hemorrhagic fever," which hit Europe in the Middle Ages and subsequently have exerted selection pressure on a gene which, today, 10% of Europeans carry a mutation of resistance to HIV infection, British researchers suggest in the "Journal of Medical Genetics."
The mutation in question, delta-32 gene in the CCR5 co-receptor for HIV, resulting in resistance to infection when it is present in two copies, and does not prevent infection but slows the progression of disease when there is only one copy.

Scientists had speculated that this mutation was present more frequently in Europe as a result of the Black Death and smallpox epidemics.

Some diseases can cause both selection pressures on genes promoting variants of these genes that help resist disease.

But researchers from the University of Liverpool, who made computer models based on demographic change in Europe between 1000 and 1800, suggest that this would mainly hemorrhagic fevers which increased the frequency of 1 / 20,000 at the time of the Black Death in the mid-14th century to the current frequency of 1/10.

According to these researchers, in fact, not the only Black Death or following outbreaks of bubonic plague or smallpox those alone can not explain the emergence of the delta-32 mutation.

However, they made the assumption that a number of alleged plague outbreaks between 1347 and 1665 are not the real plague caused by the bacterium Yersinia pestis, but would be related to a virus giving highly lethal hemorrhagic fevers. They were called "hemorrhagic plagues."

This virus would have used the CCR5 receptor have worked, with successive epidemics, a selection pressure on the delta-32 mutation for passing 1:20,000 to 1/10.

And the 17th and 18th centuries, it was smallpox that have taken over when the "hemorrhagic fever" has decreased in Western Europe.

This "hemorrhagic fever" has however persisted in northern Europe and east, and according to Professor Christopher Duncan of the University's School of Biological Sciences in Liverpool, one of the authors of the study, this "selection pressure continue "in these countries" why [the delta-32 mutation] has its highest frequency in Scandinavia and Russia. "

The consequence of this theory, if true, is that because different viruses use the same receptor or co-receptor CCR5, a part of the population enjoys today to protect themselves from HIV mutation that emerged there several centuries ago during outbreaks of other diseases.