For example, in 1665, the plague hit a small village in England called Eyam. The town quarantined itself to keep the Black Death from spreading into the rest of the country. A year later, the plague had burnt itself out but half of the townspeople were dead. Was there something special about the half that lived?
In 1996, researchers tracked down descendants of the people of Eyam and looked for any mutations they might have in common to explain this high survival rate. What they found was a mutation called CCR5-delta 32.
The CCR5-delta 32 mutation was already known for a different reason—people with one copy of the CCR5-delta 32 mutation are resistant to HIV, the virus that causes AIDS. People with 2 copies are virtually immune to HIV.
 The spread of the black death |
The CCR5-delta 32 mutation probably arose a few thousand years ago in Northeastern Europe. It stayed rare until around 700 years ago when it suddenly became more common. The plague started in Europe around 700 years ago.
So, does CCR5-delta 32 protect people from the plague bacteria? Probably not. Mice infected with the plague bacteria died at around the same rates whether or not they had the CCR5-delta 32 mutation.
Why then is this mutation so common in Europeans and even more common in people whose ancestors came from Eyam?
Maybe smallpox is the reason. Smallpox killed 3 in 10 infected people for thousands of years in Europe. Recent studies suggest that smallpox, like HIV, can’t infect someone with the CCR5-delta 32 mutation.
Of course this doesn’t explain Eyam (unless there was a lot of smallpox in the area). A more controversial theory is that an unknown virus, not the plague bacteria, caused the Black Death. Besides the evidence of the CCR5-delta 32 mutation itself, some people contend that the disease shouldn’t have been stopped by quarantine and that it spread too quickly for a flea borne illness.
Anyway, as you can see, while genetics were probably involved, there isn’t yet a solid answer as to what genes were involved.
