HIV/AIDS: gene variation could have made us vulnerable (updated)
Senate passes USD 48b bill to curb AIDS
Thu, 17 Jul 2008 09:15:43
The US Senate has approved spending USD 48 billion over the next five years to fight the spread of AIDS, tuberculosis and malaria worldwide.
The Senate voted on Wednesday to triple spending for a much-acclaimed program, which is USD 18 billion more than what US President George W. Bush has requested. Bush praised lawmakers for passing what he called a 'life-saving legislation'. The US president has been a strong advocate for the global AIDS program mainly in Africa.
"This bill will expand American leadership on global health and foster hope around the world. Once fully funded, it will not only help poor countries but serve America's interests as well," said Paul Zeitz, executive director of the Global AIDS Alliance. "We've been negotiating this legislation for many months and it is a product of bipartisan compromise and commitment to saving lives worldwide," Senator Joseph Biden, chairman of the foreign relations committee, said in a statement.
The US along with a number of countries around the world, including Sudan, Saudi Arabia, Libya and Russia, has banned travel and immigration for HIV-positive people. MSM/MMN
As relentless research on HIV/Aids continues, a new report suggest Human Beeing could have experienced a gene variation - called a SNP- that risked more frecuent infection.
Gene Variation May Raise Risk of H.I.V., Study Finds By NICHOLAS WADE Published: July 17, 2008
A genetic variation that once protected people in sub-Saharan Africa from a now extinct form of malaria may have left them somewhat more vulnerable to infection by H.I.V., the virus that causes AIDS. The gene could account for 11 percent of the H.I.V. infections in Africa, explaining why the disease is more common there than expected, researchers based in Texas and London say. The researchers said their finding had no immediate public health consequences. But if confirmed, it would offer an important insight into the biology of the virus.The genetic variation has been studied in United States Air Force personnel, whose H.I.V. infections have been followed for 25 years. African-Americans who carried the variation were 50 percent more likely to acquire H.I.V. than African-Americans who did not, although their disease progressed more slowly, say researchers led by Sunil K. Ahuja, director of the Veterans Administration H.I.V./AIDS Center, San Antonio, and Matthew J. Dolan of the Uniformed Services University in Bethesda, Md. Their results were reported Wednesday in the journal Cell Host & Microbe.
David B. Goldstein, geneticist who studies H.I.V. at Duke University, said that the new result “would be pretty exciting if it holds up” and that many other researchers would now test it. “If the results are confirmed, it would mean that selection for resistance to malaria has created a vulnerability to infection with HIV-1,” he said, referring to the principal form of the virus.
The genetic variation, called a SNP, or snip, involves a change in one unit of DNA. This particular snip has a far-reaching consequence. It prevents red blood cells from inserting a certain protein on their surface. The protein is called a receptor because it receives signals from a hormone known as CCL5, which is part of the immune system’s regulatory system.
The receptor is also used by a malarial parasite called Plasmodium vivax to gain entry to the red blood cells it feeds on. About 10,000 years ago, people in Africa who possessed the SNP variation gained a powerful survival advantage from not being vulnerable to the ancestor of Plasmodium vivax. The SNP eventually swept through the population and the vivax parasite died out in Africa, to be replaced by its current successor, Plasmodium falciparum.
More than 90 percent of people in Africa now lack the receptor on their red blood cells, as do about 60 percent of African-Americans. The possibility that the receptor has a bearing on H.I.V. infection first occurred to Robin Weiss, a biologist at University College, London, after he noticed that the virus seemed to be hitchhiking on red blood cells. Dr. Weiss, who wrote the new report with Dr. Ahuja and Dr. Dolan, showed in laboratory tests that H.I.V. latches onto the receptor in place of its intended guest, the CCL5 hormone.
The Texas-London research team is not certain how lack of the receptor promotes H.I.V. infection, but Dr. Ahuja said the red blood cells acted like a sponge for CCL5. Because CCL5 is known to obstruct multiplication of the virus, having lots of the hormone in the bloodstream may prevent infection. Conversely, people whose blood cannot soak up the hormone could be more vulnerable.
Dr. Weiss said the red blood cell receptor was similar to another receptor, CCR5, which occurs on the surface of the white blood cells that are H.I.V.’s major target. A small percentage of Europeans have a mutation that prevents the CCR5 receptor from being displayed on the surface of white blood cells, and they are protected against H.I.V.
It is somewhat puzzling that the absence of the two receptors has the opposite effect — vulnerability to H.I.V. when the red cell receptor is missing, protection from it when the white cell receptor is withdrawn. The researchers offer an explanation that they concede is far from straightforward.
“If you found the paper plain sailing, most of my students didn’t,” Dr. Weiss said. As is often the case with provocative new findings, the researchers may have some way to go before convincing others that their observation is correct. Dr. Goldstein said that in parts of the United States, African-Americans have a higher infection rate than European-Americans, and that patients with a higher proportion of African genes may be more vulnerable to H.I.V. for reasons unconnected to the SNP. Nonetheless, the SNP would show up in a greater proportion of infected people simply because of their African heritage. If so, the gene’s apparent association with H.I.V. infection could be just coincidental, not causal.
The researchers took steps to rule out this possibility, but Dr. Goldstein said those steps might not have been adequate.
Dr. Carl Dieffenbach, director of the AIDS division of the National Institute of Allergy and Infectious Diseases, said the new finding, if confirmed, would be intriguing because it pointed to the many ways in which pathogens have shaped the body’s receptors.
Although H.I.V. is too recent an infection to have left an evolutionary mark on the genome, human ancestors would have been exposed to malarial parasites and to S.I.V., which infects monkeys, and the genome still bears the marks of these challenges to survival. Better knowledge of these adaptations will help understand the biology of H.I.V. infection, he said.
Useful site: UNAIDS
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