Fact: AIDS is stopped by a gene in some people. Where is the gene therapy for that...?
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Throughout the history of the AIDS epidemic, a few lucky people have avoided infection despite being exposed again and again. Now, researchers are traveling back in evolutionary time to understand why some people are resistant -- and in some cases virtually immune -- to the AIDS virus. Studies released this week and last year suggest that the roots of AIDS immunity extend back for centuries, long before the disease even existed. Our ethnic backgrounds and the illnesses suffered by our distant ancestors appear to play a crucial role in determining whether our genes will allow HIV to take hold in our bodies. For now, the findings seem likely to inspire more raised eyebrows than cutting-edge drugs. But over time, the research into why some people don't get HIV may help doctors treat those who do. By understanding which genes help people fight off infection, "we might move to a time where we can make more refined decisions about timing or intensity of therapy. Now, it's like a glove where one size fits all," said Dr. Matthew Dolan, an AIDS specialist in the U.S. Air Force and co-author of a new AIDS genetics study in an online edition of the journal Science. Genetic resistance to AIDS works in different ways and appears in different ethnic groups. The most powerful form of resistance, caused by a genetic defect, is limited to people with European or Central Asian heritage. An estimated 1 percent of people descended from Northern Europeans are virtually immune to AIDS infection, with Swedes the most likely to be protected. One theory suggests that the mutation developed in Scandinavia and moved southward with Viking raiders. All those with the highest level of HIV immunity share a pair of mutated genes -- one in each chromosome -- that prevent their immune cells from developing a "receptor" that lets the AIDS virus break in. If the so-called CCR5 receptor -- which scientists say is akin to a lock -- isn't there, the virus can't break into the cell and take it over. To be protected, people must inherit the genes from both parents; those who inherit a mutated gene from just one parent will end up with greater resistance against HIV than other people, but they won't be immune. An estimated 10 percent to 15 percent of those descended from Northern Europeans have the lesser protection. Using formulas that estimate how long genetic mutations have been around, researchers have discovered that the mutation dates to the Middle Ages. (Similar research in mitochondrial DNA -- passed along by women -- has suggested that Europeans are all descended from seven Ice Age matriarchs.) Why would the mutation stick around so long instead of giving up the ghost? Researchers initially thought the mutation provided protection against the bubonic plague that caused the Black Death in Europe. Those with the mutation would have lived longer and had more children while many of their neighbors died off. The fact that the genetic mutation also provided protection against HIV centuries later would just be a coincidence. The plague scenario has been largely discarded in favor of another deadly scourge. "A disease like smallpox that has been continuous since that time ... is more likely," said Yale University professor of epidemiology Alison Galvani, who co-wrote a study about the possible smallpox link in 2003. According to Galvani, while the plague came and went, smallpox stuck around well into the 20th century, providing even more incentive for a protective gene to live on: It would keep people alive generation after generation, instead of just during one brief epidemic.
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Answer:
Just because they can locate information on a gene doesn't mean that replacing it in a living person is that easy. It's not like you can do a cut and paste job on every living cell in your body, and that's what you would need to do here. Every cell in your body contains a copy of your genetics, even if the cell does nothing with most of the information. Right now, it's about all the researchers can do to make glow in the dark puppies. They can insert some genetic information at the embryonic level. They can't quite do the same thing with a fully developed human. It's intriguing information no doubt, but not necessarily useful at the moment. And until they manage to figure out how to insert the desired info into your genes throughout your entire body, it's going to be that way.
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Other answers
There has been a ton of research into the CCR5 (delta 32) mutation. There is actually a case of a man who was HIV+ being treated with the stem cells of a resistant donor and the HIV-1 virus could no longer be detected in the blood, marrow, or mucous. While it didn't completely "clear" the virus from the body, the viral load dropped to such a low level that it was virtually undetectable (and probably unspreadable). Very interesting stuff! I think the problem is that - in spite of identifying the gene mutation, genetics just isn't advanced enough to mimic the resistance in a living person. But, could they CAUSE the mutation? Maybe! (But experimenting on babies is a no no)... There are a couple of articles in the New England Journal of Medicine that you might want to check out. I'm pretty sure they're paid downloads, but maybe this news brief will point you in the right direction. http://www.aidsmedication.net/?p=441
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