Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.
Important note: Information in this article was accurate in 1998. The state of the art may have changed since the publication date.
Reuters NewMedia - Wednesday September 23, 1998
Maggie Fox, Health and Science Correspondent
They said nearly a third of African-Americans had the mutation, which slows the progression from HIV infection to full-blown AIDS by an average of 3.8 years. It is the fourth mutation found to interfere with the HIV virus and is the most common in the population, Dr. David McDermott of the National Institute of Allergy and Infectious Diseases (NIAID), said.
"It may explain some of the long-term non-progressors," McDermott said, referring to people who are infected with HIV but who do not show any symptoms for years.
The mutation affects CCR5 -- a receptor, or kind of chemical doorway, that the HIV virus has to use to get into the immune system cells that it infects. People who have one or two copies of the mutated gene produce less CCR5, so the virus has less opportunity to get into their cells.
McDermott's team studied several hundred people considered at high risk of HIV infection. Of them, 414 became infected.
Two of the previously known genetic mutations delayed the progression to AIDS by about a year, but the new mutation slowed it by 3.8 years on average.
McDermott's team screened random samples from blood donors in the general population and found that 32 percent of blacks, 28 percent of Asians, 18 percent of whites and 10 percent of Hispanics had the new mutation.
The first mutation that was found also affects CCR5, and in fact people who have two copies of that variant gene produce none of the chemical receptor at all. It affects up to 15 percent of whites but not blacks or Asians.
The second mutation affects a similar receptor known as CCR2. It is found in as many as 25 percent of Americans, of all races, and has also been found to protect around 20 percent of Africans in some studies conducted there.
A third mutation in the SDF1 gene protects about five percent of people who have two copies of that mutated gene.
McDermott said the new CCR5 mutation protected people whether they had two or just one copy of the gene. He also said some people could have a combination of the four mutations.
Now his team is checking to see whether people who have the mutation respond differently to HIV drugs. An obvious next step is to see whether a drug can mimic the effects of the gene.
"It obviously wouldn't be a cure. It would just be a slowing of the progression," McDermott, whose team reported their findings in the Lancet medical journal last week, but who issued a statement on Wednesday, said.
Such a drug would be different from all the other drugs, which target the virus itself. The HIV virus mutates very quickly to resist drugs, but something that targets a human protein would be less subject to this quick evolution.
In fact, blocking CCR5 altogether could be one approach. People with two copies of the first CCR5 mutation, known as delta 32, produce no CCR5 at all. "Current knowledge is they have no medical problems," McDermott said.
Therefore, CCR5 may not be necessary to the body. The only thing known to use CCR5 is HIV. "As far as we know HIV is the only infectious agent that uses CCR5 to get into cells," McDermott said in a telephone interview.
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