[snip] The village of Eyam
It’s hard to prove the causative agent was a virus because of course in those days there were no blood tests for viruses. And today it’s impossible to extract viral DNA from 700 year-old skeletal remains. But in the last few years some evidence has emerged that seems to support the viral theory.
There may not have been blood tests, but in England at least there were parish records from about 1540. They give a detailed picture of what happened to the inhabitants of even the smallest village — births, deaths, marriages, and baptisms. One such village was Eyam, a lead-mining village in the county of Derbyshire in an area known as the Peak District, in central England.
The Black Death suddenly struck this tiny village in September 1665. The town’s rector persuaded the villagers to quarantine themselves to prevent the disease from spreading through the region. During the period of isolation, food was left for the villagers at a well on the parish boundary high up on the hill above the village, and paid for by coins which were dipped in vinegar to disinfect them. It seemed to work, because none of the surrounding areas were affected by the plague. A year later, the first outsiders ventured into Eyam. About half the town had survived.
Genetics to the rescue
In 1996, researchers from the National Institutes of Health in Washington D.C. led by Dr Stephen J O’Brien, tracked down the modern day descendents of Eyam from parish records and tested their DNA. They were curious to know whether the survivors shared any genetic similarity that had helped their ancestors resist the plague. They found high levels of a gene mutation called CCR5-delta 32 amongst the descendents. CCR5 is a gene that codes for a protein on the surface of white blood cells which acts as a receptor for other molecules involved in inflammation
These researchers knew about this protein from previous research on HIV which showed that HIV can slip past the protein, using it as a gateway to get inside and kill white cells. But people who have the mutated form of the gene — CCR5-delta 32 — don’t have this protein and their white cells won’t allow HIV in. So people with the mutation are resistant to HIV infection — they either don’t get HIV at all or are much slower to get it than people who have the normal gene.
Here was the mutation showing up again in the population of Eyam. And not just Eyam. Areas of Europe that had been affected by the plague (including America, which was mostly settled by European plague survivors and their descendents) also had unusually high levels of CCR5-delta 32 — about fourteen per cent of the population compared to two percent in areas that never experienced the Black Death — such as Asia and Africa.
The big jump in the percentage of the population with the mutation has been calculated to have occurred around 700 years ago — around the time of the first major plague epidemic, say Duncan and Scott.
It appears that, beginning 700 years ago, the Black Death increased the genetic frequency of CCR5-delta 32 mutation in the Caucasian gene pool. This protected these populations from later epidemics of both the Black Death and also HIV. The populations of Asia, and Africa had no such protection — and this also explains why HIV/AIDS has spread more quickly there. It also appears that, like HIV, the Black Death was caused by a virus, say Duncan and Scott.
They say that during the period of the Great Pestilence there were probably two separate plagues — a viral haemorrhagic fever in Europe, the Black Death; and a bubonic plague in Asia and parts of the Mediterranean coast caused by Yersinia.
The plague and globalisation
Both epidemics are examples of an evolutionary struggle that has gone on for millions of years between disease causing micro-organisms and hosts. If a micro-organism mutates into a form that makes transmission easier — to a new host for example — then it has the advantage. If the host in turn develops a mutation that protects it from the micro-organism, or develops immunity to it, then it has an advantage over that micro-organism.
The Black Death, dying out in the 17th century, lost the fight. The last great epidemic was in 1670 — after that smallpox took over as the number one infectious disease killer. [/snip]
https://www.abc.net.au/science/articles/2004/01/22/2857189.htm
