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Tytuł pozycji:

CCR5∆32 and SDF1 3'A: Gene Variants, Expression and Influence on Biological Markers for the Clinical Progression to AIDS among HIV-1 Virus Controllers in a Mixed Population of the Amazon Region of Brazil.

Tytuł:
CCR5∆32 and SDF1 3'A: Gene Variants, Expression and Influence on Biological Markers for the Clinical Progression to AIDS among HIV-1 Virus Controllers in a Mixed Population of the Amazon Region of Brazil.
Autorzy:
Lima ÉRG; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Queiroz MAF; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Lima SS; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Machado LFA; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Cayres-Vallinoto IMV; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Vallinoto ACR; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Figueiredo FAPL; Human and Medical Genetics Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Guerreiro JF; Human and Medical Genetics Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Guimarães Ishak MO; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Ishak R; Virus Laboratory, Institute of Biological Sciences, Federal University of Pará, Belém 66075-110, Brazil.
Źródło:
International journal of molecular sciences [Int J Mol Sci] 2023 Mar 04; Vol. 24 (5). Date of Electronic Publication: 2023 Mar 04.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: Basel, Switzerland : MDPI, [2000-
MeSH Terms:
Acquired Immunodeficiency Syndrome*/genetics
Chemokine CXCL12*/genetics
HIV Infections*
Receptors, CCR5*/genetics
Female ; Humans ; Male ; Biomarkers ; Brazil ; Disease Progression ; Gene Frequency ; HIV-1 ; Viremia
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Grant Information:
#301869/2017-0; #312979/2018-5; #314209/2021-2 National Council for Scientific and Technological Development; FAPESPA/PRONEX-060/2020 Fundação Amazônia Paraense de Amparo a Estudos e Pesquisas; PAPQ/2019 Federal University of Para
Contributed Indexing:
Keywords: CCR5; HIV-1; SDF1; gene variants; viremia controller
Substance Nomenclature:
0 (Biomarkers)
0 (Chemokine CXCL12)
0 (Receptors, CCR5)
0 (CXCL12 protein, human)
0 (CCR5 protein, human)
Entry Date(s):
Date Created: 20230311 Date Completed: 20230315 Latest Revision: 20230315
Update Code:
20240104
PubMed Central ID:
PMC10003039
DOI:
10.3390/ijms24054958
PMID:
36902388
Czasopismo naukowe
CCR5Δ32 and SDF1-3'A polymorphisms were investigated in a cohort of viremia controllers, without the use of therapy, along with their influence on CD4+ T lymphocytes (TLs), CD8+ TLs, and plasma viral load (VL). The samples were analyzed from 32 HIV-1-infected individuals classified as viremia controllers 1 and 2 and viremia non-controllers, from both sexes, mostly heterosexuals, paired with 300 individuals from a control group. CCR5∆32 polymorphism was identified by PCR amplification of a fragment of 189 bp for the wild-type allele and 157 bp for the allele with the ∆32 deletion. SDF1-3'A polymorphism was identified by PCR, followed by enzymatic digestion (restriction fragment length polymorphism) with the Msp I enzyme. The relative quantification of gene expression was performed by real-time PCR. The distribution of allele and genotype frequencies did not show significant differences between the groups. The gene expression of CCR5 and SDF1 was not different between the profiles of AIDS progression. There was no significant correlation between the progression markers (CD4+ TL/CD8+ TL and VL) and the CCR5∆32 polymorphism carrier status. The 3'A allele variant was associated with a marked loss of CD4+ TLs and a higher plasma VL. Neither CCR5∆32 nor SDF1-3'A was associated with viremia control or the controlling phenotype.
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