Resource: HIV Immunity
Media Type:
QuickTime Video
Length: 6m 43s
Size: 8.8 MB
Teachers' Domain, HIV Immunity, published September 26, 2003, retrieved on ,
http://www.teachersdomain.org/resource/tdc02.sci.life.gen.hivimmunity/
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During that same year, competing scientific groups made a series of discoveries that could open a new chapter in treating -- and preventing -- infection by the lethal organism. For the first time, the treatments would be aimed not at the virus itself, but at a portal through which HIV enters white blood cells and attacks the immune system.
Scientists in 1996 identified the portal: It was a large protein called Chemokine Receptor 5, or CCR-5, which is a normal part of the cell produced by a gene having the same name.
When this gene mutates, it produces the protein incorrectly. In fact, when people inherit two copies of the mutant CCR-5 gene, the cell fails to make the portal protein at all. It simply does not exist, and the cell is like a house with no front door.
The finding was "pretty stunning," said Stephen O'Brien of the National Cancer Institute. He had been searching for years for genetic changes that conferred HIV resistance, and here was a powerful one.
Perhaps best of all, people can get along fine without a functioning CCR-5 gene or protein. That makes CCR-5 an excellent "target" for drugs. A compound that blocks the CCR-5 protein might prevent HIV infection as if a person had naturally inherited the mutation.
This discovery has not yet translated into new treatments. A dozen pharmaceutical companies, however, are developing drugs designed to block HIV's entrance into the white blood cell by creating a non-functional CCR-5 receptor. Already, some of them are in clinical trials in HIV patients, perhaps laying the groundwork for the most effective treatments yet.
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Source: NOVA: "Surviving AIDS"
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