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CCR5 Genetic Variation Responsible for Resistance to HIV Might Decrease Resistance to West Nile Virus, Study Says

January 18, 2006

People living with a genetic variation in the CCR5 receptors of their immune cells -- which has shown resistance to HIV -- might have an increased risk of contracting West Nile virus, according to a study published in the Jan. 17 online edition of the Journal of Experimental Medicine, Reuters reports. People with the variation, called a CCR5-delta-32 mutation, often are less easily infected by HIV because their immune cells "lac[k] a receptor" that is thought to be used by the virus to "dock onto immune system cells and infect them," according to Reuters. People with CCR5 mutations still can contract HIV, Reuters reports. Philip Murphy, acting chief of the Laboratory of Molecular Immunology at the National Institute of Allergy and Infectious Diseases, and colleagues found that genetically engineered mice that lack CCR5 receptors are more likely to become ill or die when infected with West Nile virus than other mice. The researchers then tested blood and spinal fluid samples of 395 people who contracted West Nile in Arizona and Colorado in 2003 and 2004 (Reuters, 1/17). According to the study, 4.2% of whites in the Arizona group and 8.3% of whites in the Colorado group had the CCR5-delta-32 mutation (Glass et al., Journal of Experimental Medicine, 1/17). In the U.S., only about 1% of whites are estimated to have the CCR5-delta-32 mutation (United Press International, 1/18). The researchers also found a statistically significant association between CCR5-delta-32 mutation and the mortality rate of the West Nile patients in Arizona. "We conclude that CCR5 mediates resistance to symptomatic [West Nile] infection," the study says (Journal of Experimental Medicine, 1/17). Murphy said, "The findings may have important clinical implications for physicians who treat people with HIV," such as strictly limiting mosquito exposure to HIV-positive people who are taking experimental CCR5 inhibitors (NIH release, 1/17).

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