Evaluation of CCR5-Δ32 mutation among individuals with high risk behaviors, neonates born to HIV-1 infected mothers, HIV-1 infected individuals, and healthy people in an Iranian population

被引:6
作者
Donyavi, Tahereh [1 ]
Bokharaei-Salim, Farah [2 ]
Nahand, Javid Sadri [2 ]
Garshasbi, Saba [1 ]
Esghaei, Maryam [2 ]
Sadeghi, Mohsen [1 ]
Jamshidi, Sogol [2 ]
Khanaliha, Khadijeh [3 ]
机构
[1] Iran Univ Med Sci, Hlth, Tehran, Iran
[2] Iran Univ Med Sci, Sch Med, Dept Virol, Tehran, Iran
[3] Iran Univ Med Sci, Res Ctr Pediat Infect Dis, Inst Immunol & Infect Dis, Tehran, Iran
关键词
chemokine receptor R5 (CCR5); human immunodeficiency virus-1 (HIV-1); Iran; IMMUNODEFICIENCY-VIRUS TYPE-1; SERONEGATIVE INDIVIDUALS; DISEASE PROGRESSION; GENETIC POLYMORPHISMS; HOST DETERMINANTS; DELTA-32; MUTATION; DELETION ALLELE; HIV-1; INFECTION; CCR5; CHEMOKINE;
D O I
10.1002/jmv.25658
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
One of the important genetic factors related to resistance to HIV-1 infection is the presence of the C-C chemokine receptor type 5 delta 32 (CCR5-Delta 32) homozygous genotype (Delta 32/Delta 32). The aim of this study was to evaluate the CCR5-Delta 32 mutation among individuals with high-risk behaviors, neonates born to HIV-1-infected mothers in the prevention of mother-to-child transmission (PMTCT) project, HIV-1-infected individuals, and healthy people. The frequency of the CCR5-Delta 32 genotype was assessed in a cross-sectional survey carried out from March 2014 to March 2019 among four different groups of the Iranian population. Genomic DNA was extracted from peripheral blood mononuclear cells of 140 Iranian healthy people, 84 neonates born to HIV-1-infected mothers in the PMTCT project, 71 people with high-risk behaviors, and 76 HIV-1-infected individuals. The polymerase chain reaction method was used for the amplification of the CCR5 gene. The CCR5-Delta 32 heterozygous deletion was detected in five (6.6%) HIV-1-infected individuals, four (4.7%) neonates born to HIV-1 positive mothers, two (1.4%) healthy people, and also three (4.2%) people with high-risk behaviors whereas the CCR5-Delta 32 homozygous deletion was absent in all the groups (Fisher's exact test, P = .0242). The allele of CCR5-Delta 32 homozygous was not detected in the four study groups, and no significant difference was seen in the frequency of the CCR5 Delta 32 heterozygous allele between HIV seropositive and seronegative individuals. Therefore, it seems that this allele alone cannot explain the natural resistance to HIV-1 infection and probably several mechanisms are responsible for these processes and it should be further investigated.
引用
收藏
页码:1158 / 1164
页数:7
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