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Thu Mar 10, 2:23 PM ET Health - Reuters
LONDON (Agence de Presse Medicale) - The persistent epidemics of hemorrhagic fever that struck Europe during the Middle Ages provided the selection pressures that have made 10 percent of Europeans resistant to HIV (news - web sites) infection, according to a UK study.
A mutation called delta-32 in the cellular receptor dubbed CCR5 protects against HIV infection, and is found more often in Europeans than other populations.
Scientists have previously suggested that the genetic mutation became common because it protected people against the Black Death or smallpox epidemics, while those with normal CCR5 were wiped out.
But researchers at the University of Liverpool in England said computer modeling, based on the changing demographics of Europe from 1000 to 1800 AD, showed how hemorrhagic fever forced up the frequency of this mutation from 1 in 20,000 at the time of the Black Death to values today of 1 in 10.
The researchers note in the Journal of Medical Genetics that lethal, viral hemorrhagic fevers were recorded in the Nile valley from 1500 BC and were followed by the plagues of Mesopotamia (700-450 BC), the plague of Athens (430 BC), the plague of Justinian (AD 541-700) and the plagues of the early Islamic empire (AD 627-744).
The European plagues from 1347 to 1665 were also a continuing series of hemorrhagic infections caused by a virus that used the CCR5 as an entry port into the immune system, the researchers explain.
Although plague passed its peak after the Great Plague of London in 1665, the researchers said it did not disappear completely.
Professor Christopher Duncan, from the University's School of Biological Sciences, added: "Hemorrhagic plague did not disappear after the Great Plague of London in 1665-66 but continued in Sweden, Copenhagen, Russia, Poland and Hungary until 1800.
"This maintenance of hemorrhagic plague provided continuing selection pressure on the mutation and explains why it (the CCR5-delta-32 mutation) occurs today at its highest frequency in Scandinavia and Russia."
SOURCE: Journal of Medical Genetics, March 2005.
LONDON (Agence de Presse Medicale) - The persistent epidemics of hemorrhagic fever that struck Europe during the Middle Ages provided the selection pressures that have made 10 percent of Europeans resistant to HIV (news - web sites) infection, according to a UK study.
A mutation called delta-32 in the cellular receptor dubbed CCR5 protects against HIV infection, and is found more often in Europeans than other populations.
Scientists have previously suggested that the genetic mutation became common because it protected people against the Black Death or smallpox epidemics, while those with normal CCR5 were wiped out.
But researchers at the University of Liverpool in England said computer modeling, based on the changing demographics of Europe from 1000 to 1800 AD, showed how hemorrhagic fever forced up the frequency of this mutation from 1 in 20,000 at the time of the Black Death to values today of 1 in 10.
The researchers note in the Journal of Medical Genetics that lethal, viral hemorrhagic fevers were recorded in the Nile valley from 1500 BC and were followed by the plagues of Mesopotamia (700-450 BC), the plague of Athens (430 BC), the plague of Justinian (AD 541-700) and the plagues of the early Islamic empire (AD 627-744).
The European plagues from 1347 to 1665 were also a continuing series of hemorrhagic infections caused by a virus that used the CCR5 as an entry port into the immune system, the researchers explain.
Although plague passed its peak after the Great Plague of London in 1665, the researchers said it did not disappear completely.
Professor Christopher Duncan, from the University's School of Biological Sciences, added: "Hemorrhagic plague did not disappear after the Great Plague of London in 1665-66 but continued in Sweden, Copenhagen, Russia, Poland and Hungary until 1800.
"This maintenance of hemorrhagic plague provided continuing selection pressure on the mutation and explains why it (the CCR5-delta-32 mutation) occurs today at its highest frequency in Scandinavia and Russia."
SOURCE: Journal of Medical Genetics, March 2005.
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