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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
Actually, it the kids had Severe Combined Immunodeficiency Disease. The problem was that the engineered gene is inserted via a viral vector, and what seems to have happened is that the virus inserted into the promoter area of a gene which, when over-active, leads to cancer. There is lots of research underway on ways to prevent this, now that we know what the problem is, and the prosects are good. It should be possible to do this sort of engineering safely in the not-too-distant future.
of course, biting monkeys is not to everyone's taste - Konrad Lorenz
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
Sex is *not* primarily for producing children... you'll produce a sprog maybe a couple of times in your life. You'll normally have sex at least a few times more than that (well maybe your church won't let you, but most people will). Sex is *fun*. Enjoy it while you're young.
Were sex purely about producing children, then the females of the species would indictate when they were fertile like almost every other species on the planet, rather than being sexually receptive all the time. Sex is also about social bonding.
Aide-toi, le Ciel t'aidera - Jeanne D'Arc.
I believe no one should have sex with someone they don't plan on marrying.
That's fine for you. It in no way means that someone who doesn't live that way deserves to be punished with disease.
Aide-toi, le Ciel t'aidera - Jeanne D'Arc.
...But the gene only stops HIV type 1. The delta 32 gene mutation would not prevent infection from HIV type 2.
From this journal:
"Human immunodeficiency virus (HIV) type 2, the second AIDS-associated human retrovirus, differs from HIV-1 in its natural history, infectivity, and pathogenicity, as well as in details of its genomic structure and molecular behavior."
Type 2 is the predominant strain of the virus in Africa, so knowledge of the delta 32 mutation will have little effect on the spread of the virus in this epidemic.
However, this discovery can still potentially lead to a vaccination/cure for HIV type 1 which is the predominant strain in Europe, and possibly other areas of the world (including the middle east and western Asia), which is still very necessary.
Steve
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
90% of the DNA is never used, and so Joe has a 90% chance of having inserted himself into a string of rubbish that will never be transcribed.
That's not quite true. Many retroviruses and retrotransposons carry their own promoter sequences with them, so they increase the chance of transcription by the cellular machinery. It gets trickier when you have something like SINES, however, which lack promoter elements. They basically cluster near LINES, which carry promoter activity, so that the SINES get transcribed along with the LINES.
Da Blog
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
The CDC (Center for Disease Control) has presented this information for years (1998 is when I first heard it from them) at their seminars for charities that work with HIV positive persons. The mass media has apparently avoided this information even thought th CDC has presented it to them, just because it wasn't newsworthy or controversial as the deaths from HIV as they could be associated to homosexuality or to drug use (considered better shock topics). They have even known and offered to many of these HIV charity members the opportunity to have testing done to determine (and join in a group study) possible suceptability to HIV based on this. All this for years...
It might be beneficial against HIV, but what if it has side-effects?
Apparently nothing too nasty, since the gene can be found several generations after the "Black Death" ceased to be epidemic.
For example, the gene that helps defend against malaria (and is prevelant amongst many of African origin) is the same gene that causes sickle-cell anaemia. The benefit probably outweighs the problem, but it shouldn't be assumed that there is "better", "worse", "above" and so on.
The interesting thing about this mutation is that it is niether dominant nore recessive with respect to the gene for haemoglobin. The best genome in a Malaria area is one normal haemoglobin gene and one mutant haemoglobin gene. Problem is that a quarter of the offspring of such a population are likely to have two normal haemoglobin genes, making them vulnerable to Malaria and a quarter are likely have two mutant haemoglobin genes, which means that their blood dosn't work very well.
The big reason we try to keep humans away from infected birds is that the flu virus breaks into eight pieces inside the cell, then reassembles. Since humans can catch H5N1 directly from birds, a person who had human flu at the same time could end up mixing the two varieties together. This is how the 1967 flu happened, and while that wasn't a 1918-level event, it did kill a lot more people than the usual annual flu.
There are worse scenarios though. You may have seen that the 1918 virus was recently sequenced, and found to be an avian flu that mutated directly into human-transmissible form, without mixing with a human flu. The mutations were fairly minor, and there is some evidence that H5N1 is following the same path. It also attacks the lungs in a similar way...most flu viruses stay in the upper respiratory tract, while H5N1 and 1918 both go deep into the lungs, and provoke a massive immune-system response that destroys the lungs. Healthy adults between the ages of 20 and 40 were the hardest hit in 1918.
There's a reason why the professionals have been screaming about this for the past several years. The fact that politicians and news media have suddenly decided to hype it after ignoring it until now shouldn't fool people into thinking the hype is all there is.
You make it sound like malaria has never been a problem in N. America, when in fact it was a serious problem in the Southeast United States. Starting around the turn of the century a series of public health campaigns effectively eliminated it. There are plenty of mosquitoes capable of carrying malaria in N. America, it's just that a very small percentage are infected.
If virus were directly transcribed from latin, the proper plural would be virii
t ml
No. There is no Latin plural. If there were, it would most likely be "virus" (4th declension) or "viri" (2nd declension). "virii" just isn't Latin, it's a joke.
http://linuxmafia.com/~rick/faq/plural-of-virus.h
From observational evidence, it isn't that people with the deletion are actually immune to HIV, it is that they are less likely to be infected at a given viral load. If a person has the deletion in both copies of the gene coding for CCR5, they still may be able to be infected with HIV - but the rate of spread is significantly decreased. It takes a critical level of the virus, and a critical proportion of infected cells, meaning that it takes time (often several years) for the syndrome to manifest.
It is rather helpful to find anything at all more about HIV - it is a confusing virus, and one that is certainly evolving along with our drug treatments for it. Research is stymied, sometimes, by the unwillingness of governements and funding bodies to confront the epidemic, based on, essentially, fear of talking about sex. More reasonably, it is also difficult to perform experiments with the virus, based on ethical and moral considerations with respect to possible test subjects....
(The moral of the story is, if you want a SARS flu vaccine, you get the Chinese government to make it....it have no qualms about injecting prisoners with `maybes.' In a Western country, one would never stand for such a violation of ones rights, and yet the West has no problem with using the results of such experiments. It is worthwile examining ones own moral view on these sorts of tests. )
You're right, there most certainly are those in the medical-historical community who argue that the precise disease may not have been yersinia pestis. The point is, there is no way to run a test on the DNA of a bacterium(or virus, if that's what it was) that was around 400 years ago. There have been inconclusive attempts to get samples from skeletal remains.
Note, from my previous post, I discussed influenza. Influenza mutates so rapidly, that even if an ancestor selected for CCR5-Delta32, modern influenza may do nothing of the sort.
Another intriguing genetic tidbit. It is widely believed that the black death selected for incidences of Downs' syndrome (which is an extra copy of chormosome 21) - witness relative population rates of Downs' syndrome vis a vis caucasian/European populations and other communities - there are significantly more individuals with the condition in caucasion/European populations.
Insanity is contagious. - Yossarian