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A survey for 32 nucleotide deletion in the CCR‐5 chemokine receptor gene (Δccr‐5) conferring resistance to human immunodeficiency virus type 1 in different ethnic groups and in chimpanzees
Author(s) -
Voevodin Alexander,
Samilchuk Elena,
Dashti Suhaila
Publication year - 1998
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/(sici)1096-9071(199806)55:2<147::aid-jmv11>3.0.co;2-f
Subject(s) - biology , genotype , mutation , virology , genetics , allele , gene
The 32 nucleotide deletion in the CCR‐5 chemokine receptor gene referred to as Δccr‐5 has been shown to confer resistance to HIV‐1. Using PCR, 1,105 human subjects and 33 common chimpanzees were genotyped attributing them to one of the three possible genotypes: wild‐type homozygote (w/w); Δccr‐5 homozygote (Δccr‐5/Δccr‐5) and Δccr‐5/wild‐type heterozygotes (Δccr‐5/w). The ethnic groups investigated included different Middle Eastern nationalities (mainly Arab) and Russians. Carriers of the Δccr‐5 mutation were found among Arabs, Iranians and Russians. The highest frequency of the mutation was seen in Russians (24.4% of the Δccr‐5 heterozygotes, allele frequency–0.1221). Surprisingly, the only Δccr‐5 homozygote identified in our study was an Egyptian. The origin of the Δccr‐5 mutation in the Middle Eastern populations, both Arab and non‐Arab, is most probably due to a gene flow from the Europeans. The frequency of the Δccr‐5 mutation in Russians is one of the highest known. It might be one of the factors contributing to a relatively slow pace of increase in the incidence of sexually acquired HIV infection in Russia. None of the chimpanzees tested was positive for Δccr‐5. Interestingly, the DNA sequence of the chimpanzee CCR‐5 gene in the region including the site of the Δccr‐5 mutation, and flanking areas, was virtually identical to the homologous human sequence, only two mismatches (silent substitutions) were found. J. Med. Virol. 55:147–151, 1998. © 1998 Wiley‐Liss, Inc.