Truemors
Over one hundred thousand years ago there was the beginning of a series of migrations out of East Africa. These bands of adventurers first travelled south and eventually north up the rivers and coastlines between the great desert to the west and the salt ocean on the east until they reached another body of water that is now the Mediterranean Sea. Here they found routes through a kinder climate and environment that allowed them to choose several directions to pursue. These are the Chronicles of Modern Man.
The migrations lasted for many millenia until finally they reached every corner of the earth. Along their journeys they met others, similar hunter-gatherers who walked upright, used tools, and could communicate. Though they were a lot alike there were enough distinctions between these ancient hominids and our travellers that little or no connubial interaction took place that had lasting effects.
Scientists have now been able to map these migrations using DNA techniques to identify genetic markers. These markers are actually changes in the DNA of our travellers and were probably unwisely termed mutations in the early days of chromosome research. Most of these mutations went unnoticed though some caused alterations in skin, hair and eye colour which would be readily recognized upon birth. The reason these genetic markers are so important in tracking our travellers is that once the change happened there was no going back. The genetics of a particular group stayed with them as they migrated (or settled) and would not have occured in the population that they left behind.
Whatever skills our travellers had, coupled with beneficial moderations to their genes, they were able to analyze and adapt better to the sudden and violent climatic and evironmental changes that brought about the destruction of their cousin hominids. By 25,000 BCE we were alone, but the genetic mutations were still happening.
Sometime after the domestication of animals and farming (10,000 BCE) came about there arose small permanent communities, longer life spans, and trade. Somewhere in what is now northeastern Europe there was an outbreak of smallpox that had devastating and long reaching results. It is thought that this virus triggered a unique change in the DNA of the afflicted survivors and their offspring, and it has been labelled as the CCR5-delta32 mutation. In a case of nature coming to the rescue this mutation was to insure that the smallpox virus would not eliminate great numbers of these same creatures again; but alas, there is more!
During the 1665 Plague epidemic the town of Eyam, England put a self imposed quarantine on themselves to save the neighbouring towns and villages. The few who survived had the delta32 allele! Discovered when genetic testing of their descendants was done it has been confirmed that this mutation protects us from the Plague as well. Eyam had an unusually high population percentage (14%) with this mutation as compared to a roughly 10% average throughout Europe, Ireland has 11.3%.
As mentioned before there is no going back for these mutants. The delta32 mutation happened in Europe and is today only found here, in western Asia, and North Africa, and of course in their descendants. What makes these geographic locations significant is another virus that the CCR5-delta32 mutation protects us from: HIV-Aids. If you have been clicking the links as you read this you will not be surprised to know that if you have two pairs or copies of this delta32 gift you almost certainly will not contract smallpox, plague, or Aids.
Unfortunately, on the continent of Africa where Aids is rampant, and where even one copy of a delta32 in the genome sequence would offer some resistance, it is not in their Genetic History to have this protection against the horrible effects of this new disease. In a harsh twist of genetic fate those who stayed in Africa also had some DNA changes, to protect against malaria some chromosomes adapted to build a resistance but had a side affect, sickle-cell anaemia. So far there are no known side effects to the CCR5-delta 32 mutation.
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