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Gene Found In Black Death Survivors Stops HIV
WindozeSux writes "According to research done by Dr. Stephen O'Brien, a mutated gene known as delta 32 found in Black Death survivor descendants, stops HIV in its tracks. In order to be immune both parents have to have the delta 32 gene. From the Article: 'In 1996, research showed that delta 32 prevents HIV from entering human cells and infecting the body. O'Brien thought this principle could be applied to the plague bacteria, which affects the body in a similar manner. To determine whether the Eyam plague survivors may have carried delta 32, O'Brien tested the DNA of their modern-day descendents...'"
. . . is another's saving trait.
This article is interesting on several levels. The fact that some people are completely immune to the disease isn't really remarkable. That's been known for quite some time. What's amazing is that this fairly basic gene (a way of bringing stuff into cells) is completely redundant. It makes me wonder how much of our cellular machinery is simply there in case another part fails.
Don't worry. I don't think there's intelligent design behind it. Just cases of plagues that have swept through populations from time to time, causing these interesting redundancies to appear.
RTFA, The Black Death isn't a cure, the gene that causes people to survive the Black Death also causes people to survive an HIV infection. (If both parents have the gene, if only one of them AIDS progression is slowed down.)
Nothing but cost, [lack of] technology, and religious fundamentalists, I think.
"[Regarding the 'cloud,'] ownership was what made America different than Russia." -- Woz
to the website. The website is about researching into the gene CCR5 related to its ability to prevent infection from the Black Death, based on the research in 1996 that showed it was able to block out HIV infection.
Initially few took up the practise. Interesting many clergymen dennounced the vaccine practise as sin. The clergy believed smallpox was god's design and all, even the children, who died of smallpox were decreed by god to so die. What finally turned the tide some years later was the adoption of the vaccine practise by a high ranking member of the British aristocracy. She (her name and title don't immediately come to mind) had her children vaccinated. The strong british caste system was momentum enough to swing favour toward vaccination.
"Academicians are more likely to share each other's toothbrush than each other's nomenclature."
Cohen
Plague doesn't cause the mutation, it SELECTS the mutation.
i.e. if you don't have the mutation, plague won't give it to you. It just won't kill you even if you don't get treated if you have the mutation.
retrorocket.o not found, launch anyway?
Nobody seems to have noticed that TFA is just a summary of a TV show. And one that doesn't seem to have that much to say about Delta 32 either. Anyway, judging from Google, Delta 32 is old news.
yes it's very old news, found this at http://www.lexiline.com/lexiline/lexi76.htm -
The August 7, 1998, German daily, Die Welt, contained an article by Susanne Horst
"Zehn Prozent der Europaeer sind vor Aids geschuetzt", summarizing the genetic findings of the national cancer center in Chicago as presented by molecular biologist Stephen J. O'Brien.
Human Gene Mutation CCR-5-delta-32
There is apparently a human gene mutation, "Mutation CCR-5-delta-32", which makes its holders nearly immune to AIDS, since this gene has no receptor for AIDS-similar viruses.
Whoever has inherited this gene from BOTH parents is fairly immune to AIDS. Whoever has inherited this gene from only ONE parent also has a good deal of immunity. (The immunity is not perfect in either case, since rare strains of AIDS can use the receptor CXCR 4).
The cure isn't "RELEASE TEH PLAGUE." The interesting bit is a gene mutation regarding CCR5 that was found to stop HIV dead in its tracks, preventing it from binding to the white blood cells. The treatment that they're working on mimics this by binding to the CCR5 receptor in white blood cells, which would block HIV from binding. Tests were done on blood samples from people with this gene mutation, and the results were always negative. The people with the gene mutation are immune to HIV.
Buffalo buffalo Buffalo buffalo buffalo buffalo Buffalo buffalo!
What finally turned the tide some years later was the adoption of the vaccine practise by a high ranking member of the British aristocracy. She (her name and title don't immediately come to mind) had her children vaccinated.
It was the Princess of Wales (though she wasn't the first, she was the person who made it popular). See the Variolation section of this page for more information. This form of vaccination had been practiced in Asia for a couple thousand years before making it to the West.
>Monogomamy is an evolutionary dead end (humans are the only animals that seem to practice it).
This is untrue. While it is somewhat of a rarity on the grand scale of things other species practice monogamy.
http://en.wikipedia.org/wiki/Monogamy
While much of your post is generally on the fringes of what we know, I can say with general certainty that the answers to these questions is "No" and "No."
For the first question, one shouldn't leap to the conclusion that the number of generations equates to evolutionary success. The two aren't necessarily related. Remember, evolution is essentially about the filling of available biological niches. The niches that humans and bacteria fill are vastly different. In light of this, calling one type of successful species "more evolved" than vastly different, yet also successful, species really carries little meaning. Perhaps a better way of putting it is this: Evolution is not forward-looking. There is no beginning, middle, or end to the evolutionary path of a species. Any species present today (simply by virtue of the fact that it has survived) is just as "evolved" as any other.
For the second question, I seriously doubt our genome will (naturally) become smaller over time. Unlike bacteria, finding the extra nutrient sources to accommodate the amount of unused DNA or non-useful protein products doesn't appear to be a selective pressure. I'd suspect that this is because such an inefficiency is relatively minor for a large multi-cellular omnivore such as us and wasn't an evolutionary driving force in the past nor will be in the future.
Lastly, I'm suspicious to call the DNA whose function remains unknown "junk DNA" as others do. Who's to say that it doesn't serve a purpose simply because we lack a theory for one? To do so reeks of scientific arrogance.
-Grym
Not when the Vatican and religious leaders have been telling them that not only do condoms not prevent HIV infection, but are laced with HIV themselves:
Still think religion in Africa helps fight HIV?
Bogtha Bogtha Bogtha
PBS ran a documentary on this a few years ago. http://www.pbs.org/wnet/secrets/case_plague/index. html
Information about the CCR5-\Delta-32 and possible links with selection events occuring with respect to the plague have been known for several years, but there is no concensus on the issue.
/not/ been seen (and if there is a paper reference that claims to do so, I would very much like to see it), is evidence that yersinia pestis and HIV actually use the same receptor, and thus the selection event even makes any sense. Given that yersinia pestis is a bacteria (albeit one with a large plasmid), and HIV a virus, this seems, at a perfunctory first thought, unlikely. However, it could be true.
/virus/), and has been with humanity for 1000s of years, could have selected for such a deletion. The catastrophic nature of the event was never has high as that of yersinia pestis, but it was recurrent throughtout generations.
What has
The article seems to imply that this deletion is only evident in the people of Eyam...as you can imagine, this is not the case. It is evident in different levels amongst ethnic groups worldwide. See Stephens et al, "Dating the Origin of the CCR5-Delta32 AIDS-resistance allele by the coalesence of haplotypes", American Journal of Human Genetics, 62: 1507-1515,1998.
Eyeballing the data, it looks like the further you get from Europe, the less likely to have high levels of the allele.
Which is odd, if the black plague is at fault. There are several theoreis as to the origin of yersinia pestis, the most common being a transfer from marmot populations in Mongolia/Inner Mongolia (they are still a resevoir of the disease...but then so are ground squirrels in California), and another hypothesis being of a sub-saharan African origin. The answer, I suspect, will never be perfectly resolved ( I blame the marmots..), but it is in precisely these orginating areas (potentially), that the humans have the lowest levels of he mutation.
There was an excellent article (whose reference I cannot currently find, I apologize), that used a population dynamics approach, and concluded that the current levels of the deletion are too high to have been caused entirely by the black death selection event - that event is too recent for such a high allelic frequency. However, a longer history of influenza (which is a
The history and biology of yersinia pestis, and HIV/AIDS are fascinating. I suggest that one does some reading on the history of governmental ineptitude and institutional discrimination surrounding both. Black Plague, San Fransisco, 1905. AIDS, San Fransisco, 1980.
Insanity is contagious. - Yossarian
...but probably not true. This has been soundly refuted (in my judgement) by a 2003 paper published at Berkeley. See reference below. CCR5-delta32 (the allele) does protect against HIV, but it's unlikely it's the result of the genetic mutations of plague survivors. More likely can be traced back to smallpox survivors from 700 years ago. Check out the ref, it's online. HIV has many strains, not just two. HIV is rapidly mutating. If you're into this topic, check out the many papers at www.cdc.gov. Marianne reference: Proc Natl Acad Sci 2003 December 9; 100(25): 15276-15279 Published online 2003 November 25. doi: 10.1073/pnas.2435085100. c2003 National Academy of Sciences "Evaluating plague and smallpox as historical selective pressures for the CCR5-[Delta]32 HIV resistance allele", by Alison P. Galvani* and Montgomery Slatkin, Department of Integrative Biology, University of California, Berkeley, CA 94720 *To whom correspondence should be addressed. E-mail: agalvani@nature.berkeley.edu. Edited by Robert May, University of Oxford, Oxford, United Kingdom Received August 8, 2003; Accepted October 3, 2003. http://www.pubmedcentral.nih.gov/articlerender.fcg i?artid=299980