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Posted by / 04-Jan-2018 14:59

Therefore, our hypothesis is that the prevalence of CCR5Δ32 allele would increase with advancing patient age.

Thus, in order to investigate if the CCR5Δ32 polymorphism could confer a selective advantage on its carriers, we compared the frequencies of the CCR5Δ32 allele between two groups of SCD patients (pediatric and adult), seen at the Pernambuco Hematology and Hemotherapy Center, HEMOPE, in Northeastern Brazil, as well as the SCD adult group and a normal control group formed by blood donors.

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. Our findings failed to demonstrate an important role of the CCR5Δ32 allele in the population sample studied here.

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A significance level of 5% was used for all the statistical tests.

The CCR5 gene was in Hardy-Weinberg equilibrium in both patient groups and controls (, resp.).

The CCR5 gene, which encodes CCR5, a Th1-cell-associated chemokine receptor, has been associated with chronic inflammatory states [12].A total of 795 DNA samples from Afro-Brazilian SCD patients between 3 months and 70 years of age (631 Hb SS, 91 Hb SC, 73 Hb S/β thalassemia; 50.4% male) followed up regularly at HEMOPE were analyzed.The HEMOPE Foundation Ethics Committee approved this study (n° 017/06), and informed consent was obtained from all participants or those legally responsible for them.Sickle cell disease (SCD) is caused by either homozygosity for the hemoglobin S (Hb S) gene (sickle cell anemia, SCA) or compound heterozygosity for Hb S and another structural hemoglobin variant or beta-thalassemia [1, 2].Hb S results from a single nucleotide substitution (GAG → GTG) at the sixth codon of the β-globin gene (HBB), which causes glutamic acid to be replaced by valine at the sixth position of the polypeptide chain [3–5].

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This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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.

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