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Genetically Modified Humans
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 effect, sickle-cell anaemia. So far there are no known side effects to the CCR5-delta 32 mutation.
*picture of a chromosome
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Caoimhin1
Dunshaggin, Ireland




Most RecentMost Recommended Comments (29)
at 01:34 on July 9th, 2008
Though I applaud the intent of this post, I feel a few important things should be pointed out:
"These markers are actually changes in the DNA of our travellers and were probably unwisely termed mutations in the early days of chromosome research."
Nah. Mutation is not only the term of art but a damn good description as well.
mu·ta·tion /myuˈteɪʃən/ [myoo-tey-shuhn] –noun
1.Biology. a.a sudden departure from the parent type in one or more heritable characteristics, caused by a change in a gene or a chromosome.
2. the act or process of changing.
"if you have two pairs or copies of this delta32 gift you almost certainly will not contract smallpox, plague, or Aids"
Wow, that is quite the blanket statement, no?
CCR5 _may_ inhibit the progression of the HIV R5 strains.
Further, "it has been hypothesized that this allele was favored by natural selection during the Black Death, or during smallpox outbreaks, but this is unlikely, given that the frequency of CCR5-Δ32 in Bronze Age samples is similar to that seen today." (http://www.ncbi.nlm.nih.gov/pubmed/16678299)
at 04:13 on July 9th, 2008
Thanks for the flag, information and additional links Futureprogress!
at 03:48 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 04:10 on July 9th, 2008
Thanks lads!
at 04:31 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff. Wow what an eye opener for us.
at 04:34 on July 9th, 2008
Aye, aye Cap'n! Thanks for the GS flag!
at 04:42 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 04:44 on July 9th, 2008
Thank you both, you are gentlemen!
at 05:32 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 06:00 on July 9th, 2008
Thanks Criticom!
at 07:01 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 07:50 on July 9th, 2008
Thanks Rahul!
at 07:23 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 07:51 on July 9th, 2008
Thank you Marcel!
at 07:44 on July 9th, 2008
Caoimhin1, great stuff. Although I'm still not quite convinced that all migration flowed in one direction, from one source. That goes against some tribal oral traditions, which have great wisdom.
at 08:13 on July 9th, 2008
Thanks PEP! There is a video about this journey of man here, the 12th section has an interview with some Navajo people you might like!
at 08:43 on July 9th, 2008
Great video link, thanks. I just watched Part 2.
Tribal traditions teach us: we are all related. Once again, science catches up to reality. ;}
Although I think that since genetics is comparatively new, as are some other recent "discoveries" later years will change the story a bit and perhaps they'll discover a different "origin" place or places. Or so the stories tell us!
at 09:55 on July 9th, 2008
I'm glad you liked the video PEP! When you're finished let me know what you think? Cheers! :)
at 07:47 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 07:52 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
at 08:16 on July 9th, 2008
Thank you for reading and flagging the story lads!
at 09:23 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
Do you know if the delta32 is/can being researched to help design a cure for Aids?
at 09:56 on July 9th, 2008
"A number of new experimental HIV drugs, called entry inhibitors, have been designed to interfere with the interaction between CCR5 and HIV, including PRO140 (Progenics), Vicriviroc (Schering Plough), Aplaviroc (GW-873140) (GlaxoSmithKline) and Maraviroc (UK-427857) (Pfizer). A potential problem of this approach is that, while CCR5 is the major co-receptor by which HIV infects cells, it is not the only such co-receptor. It is possible that under selective pressure HIV will evolve to use another co-receptor. However, examination of viral resistance to AD101, molecular antagonist of CCR5, indicated that resistant viruses did not switch to another coreceptor (CXCR4) but persisted in using CCR5, either through binding to alternative domains of CCR5, or by binding to the receptor at a higher affinity. Development of Aplaviroc has been terminated due to safety concerns (potential liver toxicity)." (http://en.wikipedia.org/wiki/CCR5)
at 10:02 on July 9th, 2008
Thank you Futureprogress for all the additional information! Now that HIV is so active it will surely want live and may evolve faster than remedies can be developed!
at 09:30 on July 9th, 2008
I don't know that for sure Kferaday, this chromosome research is ongoing. The remarkable thing about the delta32 mutation is that there is something "missing" from the chromosome not that some magic serum was added to it! Whatever is missing causes the HIV to be unable to penetrate healthy cells!
at 10:10 on July 9th, 2008
Caoimhin1, I like this story. It's good stuff.
Very interesting piece, thanks!
at 10:23 on July 9th, 2008
You're most welcome Amy, thank you kindly for the GS flag! :)
at 13:29 on January 9th, 2009
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