Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms
► Pediatric HIV-1 infection. ► We evaluated the effect of Vif-APOBEC3 system variability on progression to AIDS. ► HIV-1 Vif variants accelerate the disease progression. ► Host APOBEC3G and CUL5 alleles influence Vif variability. The APOBEC3G protein is a restriction factor that can inhibit the repl...
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| creator | De Maio, Federico A. Rocco, Carlos A. Aulicino, Paula C. Bologna, Rosa Mangano, Andrea Sen, Luisa |
| description | ► Pediatric HIV-1 infection. ► We evaluated the effect of Vif-APOBEC3 system variability on progression to AIDS. ► HIV-1 Vif variants accelerate the disease progression. ► Host APOBEC3G and CUL5 alleles influence Vif variability.
The APOBEC3G protein is a restriction factor that can inhibit the replication of HIV-1. The virus has the capacity to counteract this antiviral activity through the expression of the Vif accessory protein, which recruits a CUL5-based ubiquitin ligase complex that determines APOBEC3G proteasomal degradation. In this work we evaluated in a large pediatric cohort (i) whether single nucleotide polymorphisms of APOBEC3G and CUL5 genes (APOBEC3G H186R, APOBEC3G C40693T and CUL5 SNP6) can alter the risk of HIV-1 vertical transmission and/or the rate of progression to AIDS, (ii) the effect of HIV-1 Vif variants on the clinical course of disease, and (iii) whether the patient genotype for the studied polymorphisms could have an impact on Vif characteristics.
We found no effect of the studied APOBEC3G or CUL5 genetic variants on vertical transmission or progression to pediatric AIDS. However, we detected an association of certain Vif alterations (a one amino acid insertion at position 61 and the substitutions A62D/N/S and Q136P) with an accelerated AIDS outcome. Additionally, we observed that the APOBEC3G C40693T and CUL5 SNP6 minor alleles were correlated with substitutions in Vif motifs that are involved in the interaction with APOBEC3G and CUL5 proteins, respectively. Our results suggest that Vif alterations may contribute to a rapid AIDS onset and that Vif variability could be influenced by APOBEC3G and CUL5 polymorphisms in children. |
| doi_str_mv | 10.1016/j.meegid.2011.04.020 |
| format | Article |
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The APOBEC3G protein is a restriction factor that can inhibit the replication of HIV-1. The virus has the capacity to counteract this antiviral activity through the expression of the Vif accessory protein, which recruits a CUL5-based ubiquitin ligase complex that determines APOBEC3G proteasomal degradation. In this work we evaluated in a large pediatric cohort (i) whether single nucleotide polymorphisms of APOBEC3G and CUL5 genes (APOBEC3G H186R, APOBEC3G C40693T and CUL5 SNP6) can alter the risk of HIV-1 vertical transmission and/or the rate of progression to AIDS, (ii) the effect of HIV-1 Vif variants on the clinical course of disease, and (iii) whether the patient genotype for the studied polymorphisms could have an impact on Vif characteristics.
We found no effect of the studied APOBEC3G or CUL5 genetic variants on vertical transmission or progression to pediatric AIDS. However, we detected an association of certain Vif alterations (a one amino acid insertion at position 61 and the substitutions A62D/N/S and Q136P) with an accelerated AIDS outcome. Additionally, we observed that the APOBEC3G C40693T and CUL5 SNP6 minor alleles were correlated with substitutions in Vif motifs that are involved in the interaction with APOBEC3G and CUL5 proteins, respectively. Our results suggest that Vif alterations may contribute to a rapid AIDS onset and that Vif variability could be influenced by APOBEC3G and CUL5 polymorphisms in children.</description><identifier>ISSN: 1567-1348</identifier><identifier>EISSN: 1567-7257</identifier><identifier>DOI: 10.1016/j.meegid.2011.04.020</identifier><identifier>PMID: 21571098</identifier><language>eng</language><publisher>Kidlington: Elsevier B.V</publisher><subject>Acquired Immunodeficiency Syndrome - genetics ; Acquired Immunodeficiency Syndrome - transmission ; Adolescent ; AIDS ; alleles ; amino acids ; antiviral properties ; APOBEC-3G Deaminase ; APOBEC3G ; Biological and medical sciences ; Child ; Child, Preschool ; children ; CUL5 ; Cullin Proteins - genetics ; Cytidine Deaminase - genetics ; disease course ; Disease Progression ; Epidemiology. Vaccinations ; General aspects ; Genetic Association Studies ; Genetic Variation ; genotype ; HIV-1 ; HIV-1 - genetics ; Human immunodeficiency virus 1 ; Human viral diseases ; Humans ; Immunodeficiencies ; Immunodeficiencies. Immunoglobulinopathies ; Immunopathology ; Infant ; Infectious Disease Transmission, Vertical ; Infectious diseases ; Kaplan-Meier Estimate ; Medical sciences ; Molecular Sequence Data ; patients ; Polymorphism, Genetic ; risk ; Sequence Analysis, DNA ; single nucleotide polymorphism ; ubiquitin ; Vif ; vif Gene Products, Human Immunodeficiency Virus - genetics ; Viral diseases ; Viral diseases of the lymphoid tissue and the blood. Aids ; viruses ; Young Adult</subject><ispartof>Infection, genetics and evolution, 2011-08, Vol.11 (6), p.1256-1262</ispartof><rights>2011 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-37fb30f7d8433bfa0293346ce5ed73302f1c0b88413b4e60454ed33cf83609213</citedby><cites>FETCH-LOGICAL-c415t-37fb30f7d8433bfa0293346ce5ed73302f1c0b88413b4e60454ed33cf83609213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.meegid.2011.04.020$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27926,27927,45997</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24371270$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21571098$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>De Maio, Federico A.</creatorcontrib><creatorcontrib>Rocco, Carlos A.</creatorcontrib><creatorcontrib>Aulicino, Paula C.</creatorcontrib><creatorcontrib>Bologna, Rosa</creatorcontrib><creatorcontrib>Mangano, Andrea</creatorcontrib><creatorcontrib>Sen, Luisa</creatorcontrib><title>Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms</title><title>Infection, genetics and evolution</title><addtitle>Infect Genet Evol</addtitle><description>► Pediatric HIV-1 infection. ► We evaluated the effect of Vif-APOBEC3 system variability on progression to AIDS. ► HIV-1 Vif variants accelerate the disease progression. ► Host APOBEC3G and CUL5 alleles influence Vif variability.
The APOBEC3G protein is a restriction factor that can inhibit the replication of HIV-1. The virus has the capacity to counteract this antiviral activity through the expression of the Vif accessory protein, which recruits a CUL5-based ubiquitin ligase complex that determines APOBEC3G proteasomal degradation. In this work we evaluated in a large pediatric cohort (i) whether single nucleotide polymorphisms of APOBEC3G and CUL5 genes (APOBEC3G H186R, APOBEC3G C40693T and CUL5 SNP6) can alter the risk of HIV-1 vertical transmission and/or the rate of progression to AIDS, (ii) the effect of HIV-1 Vif variants on the clinical course of disease, and (iii) whether the patient genotype for the studied polymorphisms could have an impact on Vif characteristics.
We found no effect of the studied APOBEC3G or CUL5 genetic variants on vertical transmission or progression to pediatric AIDS. However, we detected an association of certain Vif alterations (a one amino acid insertion at position 61 and the substitutions A62D/N/S and Q136P) with an accelerated AIDS outcome. Additionally, we observed that the APOBEC3G C40693T and CUL5 SNP6 minor alleles were correlated with substitutions in Vif motifs that are involved in the interaction with APOBEC3G and CUL5 proteins, respectively. Our results suggest that Vif alterations may contribute to a rapid AIDS onset and that Vif variability could be influenced by APOBEC3G and CUL5 polymorphisms in children.</description><subject>Acquired Immunodeficiency Syndrome - genetics</subject><subject>Acquired Immunodeficiency Syndrome - transmission</subject><subject>Adolescent</subject><subject>AIDS</subject><subject>alleles</subject><subject>amino acids</subject><subject>antiviral properties</subject><subject>APOBEC-3G Deaminase</subject><subject>APOBEC3G</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>children</subject><subject>CUL5</subject><subject>Cullin Proteins - genetics</subject><subject>Cytidine Deaminase - genetics</subject><subject>disease course</subject><subject>Disease Progression</subject><subject>Epidemiology. Vaccinations</subject><subject>General aspects</subject><subject>Genetic Association Studies</subject><subject>Genetic Variation</subject><subject>genotype</subject><subject>HIV-1</subject><subject>HIV-1 - genetics</subject><subject>Human immunodeficiency virus 1</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Immunodeficiencies</subject><subject>Immunodeficiencies. Immunoglobulinopathies</subject><subject>Immunopathology</subject><subject>Infant</subject><subject>Infectious Disease Transmission, Vertical</subject><subject>Infectious diseases</subject><subject>Kaplan-Meier Estimate</subject><subject>Medical sciences</subject><subject>Molecular Sequence Data</subject><subject>patients</subject><subject>Polymorphism, Genetic</subject><subject>risk</subject><subject>Sequence Analysis, DNA</subject><subject>single nucleotide polymorphism</subject><subject>ubiquitin</subject><subject>Vif</subject><subject>vif Gene Products, Human Immunodeficiency Virus - genetics</subject><subject>Viral diseases</subject><subject>Viral diseases of the lymphoid tissue and the blood. Aids</subject><subject>viruses</subject><subject>Young Adult</subject><issn>1567-1348</issn><issn>1567-7257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2P0zAQQCMEYpeFf4DAF8QpYfyR2LkglVJ2K1VapKV7tRzH7rpK4qydLuq_xyUFbpxmpHkzY7_JsrcYCgy4-rQvemN2ri0IYFwAK4DAs-wSlxXPOSn583OOKRMX2asY9wCYAxEvswuCS46hFpfZcWWt0RPyFt2s73OM7p1FTyo41bjOTUfkBzQGvwsmRpfyyaPRtE5NwWm0WH-9Q2pokZsiUjF6nQon6qebHtDi--2X1ZJe_yaW202JRt8dex_GBxf7-Dp7YVUXzZtzvMq231Y_ljf55vZ6vVxscs1wOeWU24aC5a1glDZWAakpZZU2pWk5pUAs1tAIwTBtmKmAlcy0lGoraAU1wfQq-zjPTd94PJg4yd5FbbpODcYfohRcEF7VUCWSzaQOPsZgrByD61U4Sgzy5Fzu5excnpxLYDI5T23vzgsOTW_av01_JCfgwxlQUavOBjVoF_9xjHJM-GnQ-5mzyku1C4nZ3qVNJQAwDjVPxOeZMEnYkzNBRu3MoNNFQrqibL37_1t_AdxqqGU</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>De Maio, Federico A.</creator><creator>Rocco, Carlos A.</creator><creator>Aulicino, Paula C.</creator><creator>Bologna, Rosa</creator><creator>Mangano, Andrea</creator><creator>Sen, Luisa</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20110801</creationdate><title>Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms</title><author>De Maio, Federico A. ; Rocco, Carlos A. ; Aulicino, Paula C. ; Bologna, Rosa ; Mangano, Andrea ; Sen, Luisa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-37fb30f7d8433bfa0293346ce5ed73302f1c0b88413b4e60454ed33cf83609213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Acquired Immunodeficiency Syndrome - genetics</topic><topic>Acquired Immunodeficiency Syndrome - transmission</topic><topic>Adolescent</topic><topic>AIDS</topic><topic>alleles</topic><topic>amino acids</topic><topic>antiviral properties</topic><topic>APOBEC-3G Deaminase</topic><topic>APOBEC3G</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>children</topic><topic>CUL5</topic><topic>Cullin Proteins - genetics</topic><topic>Cytidine Deaminase - genetics</topic><topic>disease course</topic><topic>Disease Progression</topic><topic>Epidemiology. Vaccinations</topic><topic>General aspects</topic><topic>Genetic Association Studies</topic><topic>Genetic Variation</topic><topic>genotype</topic><topic>HIV-1</topic><topic>HIV-1 - genetics</topic><topic>Human immunodeficiency virus 1</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Immunodeficiencies</topic><topic>Immunodeficiencies. Immunoglobulinopathies</topic><topic>Immunopathology</topic><topic>Infant</topic><topic>Infectious Disease Transmission, Vertical</topic><topic>Infectious diseases</topic><topic>Kaplan-Meier Estimate</topic><topic>Medical sciences</topic><topic>Molecular Sequence Data</topic><topic>patients</topic><topic>Polymorphism, Genetic</topic><topic>risk</topic><topic>Sequence Analysis, DNA</topic><topic>single nucleotide polymorphism</topic><topic>ubiquitin</topic><topic>Vif</topic><topic>vif Gene Products, Human Immunodeficiency Virus - genetics</topic><topic>Viral diseases</topic><topic>Viral diseases of the lymphoid tissue and the blood. Aids</topic><topic>viruses</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>De Maio, Federico A.</creatorcontrib><creatorcontrib>Rocco, Carlos A.</creatorcontrib><creatorcontrib>Aulicino, Paula C.</creatorcontrib><creatorcontrib>Bologna, Rosa</creatorcontrib><creatorcontrib>Mangano, Andrea</creatorcontrib><creatorcontrib>Sen, Luisa</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Infection, genetics and evolution</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>De Maio, Federico A.</au><au>Rocco, Carlos A.</au><au>Aulicino, Paula C.</au><au>Bologna, Rosa</au><au>Mangano, Andrea</au><au>Sen, Luisa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms</atitle><jtitle>Infection, genetics and evolution</jtitle><addtitle>Infect Genet Evol</addtitle><date>2011-08-01</date><risdate>2011</risdate><volume>11</volume><issue>6</issue><spage>1256</spage><epage>1262</epage><pages>1256-1262</pages><issn>1567-1348</issn><eissn>1567-7257</eissn><abstract>► Pediatric HIV-1 infection. ► We evaluated the effect of Vif-APOBEC3 system variability on progression to AIDS. ► HIV-1 Vif variants accelerate the disease progression. ► Host APOBEC3G and CUL5 alleles influence Vif variability.
The APOBEC3G protein is a restriction factor that can inhibit the replication of HIV-1. The virus has the capacity to counteract this antiviral activity through the expression of the Vif accessory protein, which recruits a CUL5-based ubiquitin ligase complex that determines APOBEC3G proteasomal degradation. In this work we evaluated in a large pediatric cohort (i) whether single nucleotide polymorphisms of APOBEC3G and CUL5 genes (APOBEC3G H186R, APOBEC3G C40693T and CUL5 SNP6) can alter the risk of HIV-1 vertical transmission and/or the rate of progression to AIDS, (ii) the effect of HIV-1 Vif variants on the clinical course of disease, and (iii) whether the patient genotype for the studied polymorphisms could have an impact on Vif characteristics.
We found no effect of the studied APOBEC3G or CUL5 genetic variants on vertical transmission or progression to pediatric AIDS. However, we detected an association of certain Vif alterations (a one amino acid insertion at position 61 and the substitutions A62D/N/S and Q136P) with an accelerated AIDS outcome. Additionally, we observed that the APOBEC3G C40693T and CUL5 SNP6 minor alleles were correlated with substitutions in Vif motifs that are involved in the interaction with APOBEC3G and CUL5 proteins, respectively. Our results suggest that Vif alterations may contribute to a rapid AIDS onset and that Vif variability could be influenced by APOBEC3G and CUL5 polymorphisms in children.</abstract><cop>Kidlington</cop><pub>Elsevier B.V</pub><pmid>21571098</pmid><doi>10.1016/j.meegid.2011.04.020</doi><tpages>7</tpages></addata></record> |
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| subjects | Acquired Immunodeficiency Syndrome - genetics Acquired Immunodeficiency Syndrome - transmission Adolescent AIDS alleles amino acids antiviral properties APOBEC-3G Deaminase APOBEC3G Biological and medical sciences Child Child, Preschool children CUL5 Cullin Proteins - genetics Cytidine Deaminase - genetics disease course Disease Progression Epidemiology. Vaccinations General aspects Genetic Association Studies Genetic Variation genotype HIV-1 HIV-1 - genetics Human immunodeficiency virus 1 Human viral diseases Humans Immunodeficiencies Immunodeficiencies. Immunoglobulinopathies Immunopathology Infant Infectious Disease Transmission, Vertical Infectious diseases Kaplan-Meier Estimate Medical sciences Molecular Sequence Data patients Polymorphism, Genetic risk Sequence Analysis, DNA single nucleotide polymorphism ubiquitin Vif vif Gene Products, Human Immunodeficiency Virus - genetics Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids viruses Young Adult |
| title | Effect of HIV-1 Vif variability on progression to pediatric AIDS and its association with APOBEC3G and CUL5 polymorphisms |
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