WEDNESDAY, Jan. 18 (HealthDay News) -- A defect in the chemokine receptor CCR5 that protects against HIV increases susceptibility to West Nile virus (WNV), according to a study published online Jan. 17 in the Journal of Experimental Medicine. The finding has implications for CCR5-blocking agents under development for treating HIV/AIDS, the authors say.
Philip M. Murphy, M.D., of the National Institute of Allergy and Infectious Diseases in Bethesda, Md., and colleagues recently proved that CCR5 plays a critical role in West Nile infection in mice. In the new study, they determined the frequency of CCR5-delta32 homozygosity in patients from Arizona and Colorado with symptomatic, laboratory-confirmed WNV infection. This defective CCR5 allele, which protects against HIV infection by disabling the CCR5 receptor, is found predominantly in whites.
In the general population of U.S. blood donors, 1% of whites were homozygotic for CCR5-delta32. However, in the Arizona patients, 4.2% of whites were homozygotic for CCR5-delta32 as were 8.3% of the Colorado patients.
"CCR5-delta32 homozygosity was significantly associated with fatal outcome in the Arizona cohort. We conclude that CCR5 mediates resistance to symptomatic WNV infection. Because CCR5 is also the major HIV coreceptor, these findings have important implications for the safety of CCR5-blocking agents under development for HIV/AIDS," the authors conclude.
Abstract
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