20 April 2004
CCR5-D32 heterozygosity does not contribute to slowing disease progression in paedric AIDS
Challenging differential diagnosis, Diagnostic / therapeutic accidents, Rare disease
Susana Alvarez, Salvador Resino, Dolores Gurbindo, Angeles MuEóz-FernándezCase Rep Clin Pract Rev 2004; 5(null):51-53 :: ID: 12261
Abstract
Background: Entry of human immunodeficiency type 1 virus (HIV-1) into target cells requires both CD(4) and one chemokine receptor. Viruses predominantly use two major co-receptors, CCR5 and
CXCR4. A 32-base pair (bp) deletion mutation in the β-chemokine receptor CCR5 gene has been associated with resistance against human immunodeficiency virus type 1 (HIV-1) infection and disease.Report: We have analysed the potential protection of this mutation in the CCR5 gene (CCR5-?32) n the course of pediatric AIDS of a 12-years-old child who had the CCR5/-?32ccr5 heterozygous genotype.Conclusions: Our results indicate that it did not confer any benefit to the progression of disease in any virological and immunological markers studied.
Keywords: CCR5, progressors, HIV-1, children, AIDS
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