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http://purl.uniprot.org/citations/25548430http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25548430http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.org/dc/terms/identifier"doi:10.1155/2014/678246"xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Costa F.F."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Albuquerque D.M."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Ribeiro D.M."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Santos M.N."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Zaccariotto T.R."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Sonati M.d.e. F."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Bezerra M.A."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Araujo A.d.a. S."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Faber E.W."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Hatzlhofer B.L."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/author"Lopes M.P."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/date"2014"xsd:gYear
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http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/pages"678246"xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/title"The CCR5Delta32 polymorphism in Brazilian patients with sickle cell disease."xsd:string
http://purl.uniprot.org/citations/25548430http://purl.uniprot.org/core/volume"2014"xsd:string
http://purl.uniprot.org/citations/25548430http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25548430
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