Medieval plague may explain resistance to HIV

Key points
- The persistent epidemics of haemorrhagic fever that struck Europe during the Middle Ages provided the selection pressures that have made 10 percent of Europeans resistant to HIV 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 haemorrhagic 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 persistent epidemics of haemorrhagic fever that struck Europe during the Middle Ages provided the selection pressures that have made 10 percent of Europeans resistant to HIV 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 haemorrhagic 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 haemorrhagic 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 haemorrhagic 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: "Haemorrhagic 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 haemorrhagic 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.
Written and revised by
David Cohen, M.D.
Our doctors write and review articles for accuracy and keep them up to date.
health.am provides general information, not medical advice. Always consult a qualified health professional about your own health.
Explore health topics
More in this topic
Infections, HIV & STIs →
NewsNew tool reveals mutations that cause HIV-drug resistance
Protease inhibitor drugs are one of the major weapons in the fight against HIV, the virus that causes AIDS, but their effectiveness is limited as the virus mutates and develops resistance to the drugs over time. Now a…
9 July 2011
NewsNew report explains why physicians are reluctant to share patient data
Family doctors are reluctant to disclose identifiable patient information, even in the context of an influenza pandemic, mostly in an effort to protect patient privacy. A recently published study by Dr. Khaled El Emam…
8 July 2011
NewsDrug-resistance fears for deadly fungal disease
Deadly human fungal infections caused by certain strains of Aspergillus fungi appear to be developing resistance to current drug treatments at an alarming rate, say scientists. University of Manchester researchers,…
