A 14-month self-imposed quarantine
In late summer of 1665, a tailor in the small Derbyshire village of Eyam received a bale of cloth from London. His assistant, George Viccars, opened the damp bundle and laid it by the fire to dry, releasing fleas carrying the bacterium Yersinia pestis. Viccars was the first of many to die. The bubonic plague spread rapidly through the autumn, subsided during the winter, and returned with force the following spring.
As the death toll mounted, the village rector, William Mompesson, and the ejected Puritan minister Thomas Stanley, made an unusual proposal. They convinced the villagers to quarantine themselves to prevent the plague from reaching the surrounding towns of Sheffield and Bakewell. The quarantine began in June 1666, eight months after the initial outbreak.
The community established strict rules. They held church services outdoors at a location called Culfin Dell to allow for separation between families. They also buried their own dead in fields and gardens near their homes rather than the churchyard to hasten interment. Supplies were left for them at designated boundary stones, where the villagers would leave coins submerged in vinegar, which they believed would disinfect them.
The quarantine lasted for 14 months. By the time the last plague death occurred on November 1, 1666, 260 of the village's approximately 800 inhabitants had died. The peak mortality occurred in August 1666, when 78 people perished. One woman, Elizabeth Hancock, buried her husband and six of her children over an eight-day period, yet she herself survived.
The genetic legacy of survivors
Centuries later, the story of Eyam's self-sacrifice took a scientific turn. In 1996, researchers began a study to see if the survivors passed down a genetic advantage. They took DNA samples from modern-day descendants of the 1666 survivors, a task made possible because the village had kept parish registers since 1630. The scientists were looking for a specific genetic mutation that might explain the high survival rate in the face of near-certain exposure.
The study identified a higher-than-normal frequency of a specific genetic mutation called CCR5-delta 32 (also written as CCR5-Δ32). This mutation is a 32-base-pair deletion on human chromosome 3. The CCR5 gene provides the code for a protein receptor on the surface of white blood cells. The delta 32 mutation results in a non-functional receptor.
This specific mutation is known in another context: it provides resistance to HIV. The HIV virus uses the CCR5 receptor as a primary docking port to enter and infect host cells. Individuals with one copy of the CCR5-delta 32 mutation are resistant to HIV infection, while those with two copies are nearly immune. The theory is that this same mutation may have prevented the Yersinia pestis bacterium from successfully entering the white blood cells of the Eyam villagers who carried it. While the link between CCR5-delta 32 and plague resistance is still debated by some scientists, the allele frequency in Eyam descendants was found to be 15 percent, slightly higher than the 10 percent seen in neighboring villages.