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. Issue 8 (17th January 2020)

• Record Type: Journal Article
• Authors: Donyavi, Tahereh; Bokharaei‐Salim, Farah; Nahand, Javid Sadri; Garshasbi, Saba; Esghaei, Maryam; Sadeghi, Mohsen; Jamshidi, Sogol; Khanaliha, Khadijeh
• Is Part Of: Journal of medical virology. Volume 92:Issue 8(2020)
• Page Start: 1158
• Page End: 1164
• Publication Date: 2020-01-17
• Subjects: chemokine receptor R5 (CCR5) -- human immunodeficiency virus‐1 (HIV‐1) -- Iran; Virology -- Periodicals; 616
• DOI: 10.1002/jmv.25658
• Languages: English
• ISSNs: 0146-6615

Abstract

Abstract: 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‐Δ32) homozygous genotype (Δ32/Δ32). The aim of this study was to evaluate the CCR5‐Δ32 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‐Δ32 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‐Δ32 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‐Δ32 homozygous deletion was absent in all the groups (Fisher's exact test, P = .0242). The allele of CCR5‐Δ32 homozygous was not detected in the four study groups, and no significant difference was seen in the frequency of the CCR5Δ32 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.