alexa The Frequency and Effects of CCR5 Delta 32 Allele in Gondar Population
ISSN: 2168-9547

Molecular Biology: Open Access
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Research Article

The Frequency and Effects of CCR5 Delta 32 Allele in Gondar Population

Adugnaw Admas*

Ethiopian Environment and Forest Research Institute, Ethiopia

*Corresponding Author:
Adugnaw Admas
Ethiopian Environment and Forest Research Institute
Tel: +251-918561763
E-mail: [email protected]

Received date: June 24, 2016; Accepted date: July 07, 2016; Published date: July 14, 2016

Citation: Admas A (2016) The Frequency and Effects of CCR5 Delta 32 Allele in Gondar Population. Mol Biol 5:168. doi: 10.4172/2168-9547.1000168

Copyright: © 2016 Admas A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.



HIV is the virus that causes AIDS. Its infection occurs by binding to CD4+ receptor and chemokine receptor 5 (CCR5). Recent studies have shown that reasons for progression and non-progression are multi factorial and may involve genetic, virological and immunological factors that influence HIV disease progression in various ways. Chemokine receptors act as important co receptors mediating the entry of the human immunodeficiency virus type 1 (HIV-1) into susceptible cells. The Δ32 mutation at the CCR5 locus is a well-studied example of natural selection acting in humans. Homozygous carriers of the Δ32 mutation are resistant to HIV-1. The aim of the present study was to assess the frequency of CCR5-Δ32 (Chemokine receptor delta 32 allele) in HIV-1 untreated individuals who visited Gondar university teaching hospital. 3 ml blood samples of fifty HIV-1 untreated seropositive individual and equal numbers of age and sex match seronegative individual who are exposed and uninfected were collected using EDTA coated vacutenous tubes. DNA from 1 ml blood samples was isolated using phenol-chloroform method. Specially designed primers, both forward and reverse was used to amplify the alleles of CCR5 using PCR (Polymerase chain reaction). Desirable data regarding study subjects were collected by using specifically designed questioner. SPSS 16 and EPI-info version 3.2 were used to analyze the data. The frequency of the homozygous CCR5 mutant allele was zero in the study population and there was statistically no significance difference between the frequency of the heterozygous allele among cases and controls. There was no homozygous mutant allele both in cases and controls in the present study. This may be due to small sample size and thus another study on the same population with large sample size is warranted to further confirm the result.


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