Open AccessFrequency of CCR5-Δ32, CCR2-64I and SDF1-3'A alleles in HIV-infected and uninfected patients in Istanbul, Turkey
Author(s) -
Muammer Osman Köksal,
Baki Akgül,
Hayati Beka,
Sevgi Çıftçı,
Fahriye Keskın,
Haluk Eraksoy,
Ali Ağaçfidan
Publication year - 2021
Publication title -
journal of infection in developing countries
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.322
H-Index - 49
eISSN - 2036-6590
pISSN - 1972-2680
DOI - 10.3855/jidc.12861
Subject(s) - biology , restriction fragment length polymorphism , ccr2 , turkish population , virology , allele , population , polymerase chain reaction , allele frequency , cohort , genotype , genetics , chemokine receptor , gene , polymorphism (computer science) , immunology , chemokine , medicine , receptor , environmental health
Co-receptors involved in cell entry of the human immunodeficiency virus (HIV) and mutations in genes encoding their ligands may play a role in the susceptibility to infection and resistance to the progression of the infection. The best studied mutations that can exist in these genes are the CCR5-Δ32, CCR2-64I and SDF1-3'A mutations. The frequency of these mutations vary from continent to continent and even from region to region. However, there is limited information on their distribution throughout the Turkish population. Istanbul is the city with the highest number of documented HIV-infected patients in Turkey, which can be attributed to the population size. The aim of this study was to determine the distribution of three AIDS-related gene variants among HIV-infected and uninfected population in Istanbul, Turkey and to estimate the contribution of these variants to susceptibility or resistance to HIV.
Methodology: A total of 242 healthy individuals and 200 HIV-positive patients were included in the study. CCR5 polymorphisms were genotyped by polymerase chain reaction. CCR2 and SDF1 polymorphisms were genotyped using PCR restriction fragment length polymorphism (PCR-RFLP).
Results: The allelic frequencies for CCR5-Δ32, CCR2-64I and SDF1-3’A were 4.07%, 19.8% and 28.7%, respectively. No individual was found to carry the homozygous CCR5-Δ32 mutation in either cohort. No polymorphism was found to be significantly elevated in the HIV-infected cohort compared to the healthy group.
Conclusions: The distribution of CCR5-Δ32, CCR2-64I, and SDF1-3'A variants does not differ between HIV-infected and uninfected patients. CCR2-64I and SDF1-3'A frequencies are relatively high where as the frequency of CCR5-Δ32 is low.