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Background . Previous studies on the role of inflammation in the pathophysiology of sickle cell disease (SCD) suggested that the  CCR5Δ32  allele, which is responsible for the production of truncated C-C chemokine receptor type 5 (CCR5), could confer a selective advantage on patients with SCD because it leads to a less efficient Th1 response. We determined the frequency of the  CCR5Δ32  polymorphism in 795 Afro-Brazilian SCD patients followed up at the Pernambuco Hematology and Hemotherapy Center, in Northeastern Brazil, divided into a pediatric group (3 months–17 years,  n  = 483) and an adult group (18–70 years,  n  = 312). The adult patients were also compared to a healthy control group (blood donors, 18–61 years,  n  = 247).  Methods . The  CCR5/CCR5Δ32  polymorphism was determined by allele-specific PCR.  Results . No homozygous patient for the  CCR5Δ32  allele was detected. The frequency of heterozygotes in the study population (patients and controls) was 5.8%, in the total SCD patients 5.1%, in the children 5.4%, in the adults with SCD 4.8%, and in the adult controls 8.1%. These differences did not reach statistical significance.  Conclusions . Our findings failed to demonstrate an important role of the  CCR5Δ32  allele in the population sample studied here.

TheCCR5Δ32Polymorphism in Brazilian Patients with Sickle Cell Disease