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
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 contro...
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Veröffentlicht in: | International journal of molecular sciences 2023-03, Vol.24 (5), p.4958 |
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creator | Lima, Érica Ribeiro Gomes Queiroz, Maria Alice Freitas Lima, Sandra Souza Machado, Luiz Fernando Almeida Cayres-Vallinoto, Izaura Maria Vieira Vallinoto, Antonio Carlos Rosário Figueiredo, Fernanda Andreza de Pinho Lott Guerreiro, João Farias Guimarães Ishak, Marluísa de Oliveira Ishak, Ricardo |
description | 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. |
doi_str_mv | 10.3390/ijms24054958 |
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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.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms24054958</identifier><identifier>PMID: 36902388</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Acquired immune deficiency syndrome ; AIDS ; Alleles ; Biomarkers ; CCR5 protein ; CD4 antigen ; CD8 antigen ; Chemokines ; Controllers ; Development and progression ; Enzymes ; Gene deletion ; Gene expression ; Gene frequency ; Gene polymorphism ; Genes ; Genetic aspects ; Genetic polymorphisms ; HIV ; HIV (Viruses) ; Human immunodeficiency virus ; Infections ; Lymphocytes ; Lymphocytes T ; Mutation ; Phenotypes ; Polymorphism ; Restriction fragment length polymorphism ; SDF-1 protein ; Statistical significance ; T cells ; Viremia ; Virus diseases</subject><ispartof>International journal of molecular sciences, 2023-03, Vol.24 (5), p.4958</ispartof><rights>COPYRIGHT 2023 MDPI AG</rights><rights>2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2023 by the authors. 2023</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2968-78767db644251b4b72ba24d4fee2f158bb062e691ca2d6068eacb089cb4b8c5e3</cites><orcidid>0000-0003-1135-6507 ; 0000-0003-4321-073X ; 0000-0002-4571-4715 ; 0000-0003-1979-3656 ; 0000-0003-2014-2770</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10003039/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10003039/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids></links><search><creatorcontrib>Lima, Érica Ribeiro Gomes</creatorcontrib><creatorcontrib>Queiroz, Maria Alice Freitas</creatorcontrib><creatorcontrib>Lima, Sandra Souza</creatorcontrib><creatorcontrib>Machado, Luiz Fernando Almeida</creatorcontrib><creatorcontrib>Cayres-Vallinoto, Izaura Maria Vieira</creatorcontrib><creatorcontrib>Vallinoto, Antonio Carlos Rosário</creatorcontrib><creatorcontrib>Figueiredo, Fernanda Andreza de Pinho Lott</creatorcontrib><creatorcontrib>Guerreiro, João Farias</creatorcontrib><creatorcontrib>Guimarães Ishak, Marluísa de Oliveira</creatorcontrib><creatorcontrib>Ishak, Ricardo</creatorcontrib><title>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</title><title>International journal of molecular sciences</title><description>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.</description><subject>Acquired immune deficiency syndrome</subject><subject>AIDS</subject><subject>Alleles</subject><subject>Biomarkers</subject><subject>CCR5 protein</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Chemokines</subject><subject>Controllers</subject><subject>Development and progression</subject><subject>Enzymes</subject><subject>Gene deletion</subject><subject>Gene expression</subject><subject>Gene frequency</subject><subject>Gene polymorphism</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>HIV</subject><subject>HIV (Viruses)</subject><subject>Human immunodeficiency virus</subject><subject>Infections</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Mutation</subject><subject>Phenotypes</subject><subject>Polymorphism</subject><subject>Restriction fragment length polymorphism</subject><subject>SDF-1 protein</subject><subject>Statistical significance</subject><subject>T cells</subject><subject>Viremia</subject><subject>Virus 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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</title><author>Lima, Érica Ribeiro Gomes ; Queiroz, Maria Alice Freitas ; Lima, Sandra Souza ; Machado, Luiz Fernando Almeida ; Cayres-Vallinoto, Izaura Maria Vieira ; Vallinoto, Antonio Carlos Rosário ; Figueiredo, Fernanda Andreza de Pinho Lott ; Guerreiro, João Farias ; Guimarães Ishak, Marluísa de Oliveira ; Ishak, Ricardo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2968-78767db644251b4b72ba24d4fee2f158bb062e691ca2d6068eacb089cb4b8c5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Acquired immune deficiency syndrome</topic><topic>AIDS</topic><topic>Alleles</topic><topic>Biomarkers</topic><topic>CCR5 protein</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>Chemokines</topic><topic>Controllers</topic><topic>Development and progression</topic><topic>Enzymes</topic><topic>Gene deletion</topic><topic>Gene expression</topic><topic>Gene frequency</topic><topic>Gene polymorphism</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>HIV</topic><topic>HIV (Viruses)</topic><topic>Human immunodeficiency virus</topic><topic>Infections</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Mutation</topic><topic>Phenotypes</topic><topic>Polymorphism</topic><topic>Restriction fragment length polymorphism</topic><topic>SDF-1 protein</topic><topic>Statistical significance</topic><topic>T cells</topic><topic>Viremia</topic><topic>Virus diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lima, Érica Ribeiro Gomes</creatorcontrib><creatorcontrib>Queiroz, Maria Alice Freitas</creatorcontrib><creatorcontrib>Lima, Sandra 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Amazon Region of Brazil</atitle><jtitle>International journal of molecular sciences</jtitle><date>2023-03-01</date><risdate>2023</risdate><volume>24</volume><issue>5</issue><spage>4958</spage><pages>4958-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>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. 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subjects | Acquired immune deficiency syndrome AIDS Alleles Biomarkers CCR5 protein CD4 antigen CD8 antigen Chemokines Controllers Development and progression Enzymes Gene deletion Gene expression Gene frequency Gene polymorphism Genes Genetic aspects Genetic polymorphisms HIV HIV (Viruses) Human immunodeficiency virus Infections Lymphocytes Lymphocytes T Mutation Phenotypes Polymorphism Restriction fragment length polymorphism SDF-1 protein Statistical significance T cells Viremia Virus diseases |
title | 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 |
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