CCR2 allele polymorphisms in 15 Chinese ethnic populations

Summary Chemokine receptor‐2 (CCR2) is a co‐receptor for the entry of human immunodeficiency virus‐1 (HIV‐1) into the target cells. A mutation in CCR2 (CCR2‐64I) exhibited a protective effect to delay the progression of acquired immunodeficiency syndrome (AIDS). To study the mutant frequency and pol...

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Bibliographic Details
Published in:International Journal of Immunogenetics Vol. 33; no. 1; pp. 45 - 48
Main Authors: Zhang, X. L., Zhang, C. Y., Yu, Y., Chen, F., Li, P., Fu, S. B.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Science Ltd 01-02-2006
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Summary:Summary Chemokine receptor‐2 (CCR2) is a co‐receptor for the entry of human immunodeficiency virus‐1 (HIV‐1) into the target cells. A mutation in CCR2 (CCR2‐64I) exhibited a protective effect to delay the progression of acquired immunodeficiency syndrome (AIDS). To study the mutant frequency and polymorphism of CCR2 in Chinese populations, 1082 individuals from 15 Chinese populations distributing widely from north to south were collected. The genotypes of CCR2‐64I were determined by polymerase chain reaction–restriction fragment length polymorphism (PCR‐RFLP) with the digestion of restriction endonuclease FokI. Of the 1082 individuals, 352 (32.53%) were carriers of CCR2‐64I allele, 257 of whom (23.75%) were heterozygotes (CCR2‐64V/I), whereas 95 (8.78%) were homozygotes (CCR2‐64V/V). The frequency of the CCR2‐64I allele in those tested individuals was 20.66%. This prevalence of CCR2‐64I was higher than what was known for American and European populations. Moreover, the frequencies of CCR2‐64I were generally higher in northern China than they were in southern China, and the frequencies had significant variance in 15 populations of China (χ2 = 27.135, P = 0.018).
Bibliography:ark:/67375/WNG-DK4FWJ7W-J
istex:E404A5F521C0F84FA2B98B9FBF3A0E1FE1DC1288
ArticleID:IJI564
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1744-3121
1744-313X
1365-2370
DOI:10.1111/j.1744-313X.2006.00564.x