Chemokine Receptor Polymorphisms and Human Immunodeficiency Virus Disease Progression
The role of polymorphisms in genes encoding chemokines and their receptors (CCR2B, SDF-1, and the promoter region of CCR5) in human immunodeficiency virus (HIV) disease progression was studied in 132 white HIV type 1 (HlV-l)-infected participants from a United Kingdom cohort study. Genotyping was do...
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| Veröffentlicht in: | The Journal of infectious diseases 1999-10, Vol.180 (4), p.1096-1105 |
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| container_title | The Journal of infectious diseases |
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| creator | Easterbrook, Philippa J. Rostron, Tim Ives, Natalie Troop, Maxine Gazzard, Brian G. Rowland-Jones, Sarah L. |
| description | The role of polymorphisms in genes encoding chemokines and their receptors (CCR2B, SDF-1, and the promoter region of CCR5) in human immunodeficiency virus (HIV) disease progression was studied in 132 white HIV type 1 (HlV-l)-infected participants from a United Kingdom cohort study. Genotyping was done by use of amplification refractory mutation system-polymerase chain reaction with sequence-specific primers, and Cox proportional hazards models were used to examine the impact of polymorphisms on time to a CD4 cell count |
| doi_str_mv | 10.1086/314997 |
| format | Article |
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Genotyping was done by use of amplification refractory mutation system-polymerase chain reaction with sequence-specific primers, and Cox proportional hazards models were used to examine the impact of polymorphisms on time to a CD4 cell count <200 × 106/L and to CDC stage IV disease. The results confirm a significant association of the CCR2B-64I mutant genotype with slower progression to a CD4 count <200 (hazards ratio [HR], 0.39; 95% confidence interval [CI], 0.17–0.91) but not with the SDF-lα 3′ UTR homozygous mutation. The effects of the CCR5 and CCR2 mutations were genetically independent and similar in the magnitude of their protective effect on progression to a CD4 count <200 cells. A novel finding was an association of borderline significance between homozygosity for C at nucleotide position 59353 in the CCR5 promoter region and a slower rate of CD4 cell decline to <200 × 106/L (HR, 0.58; 95% CI, 0.34–0.996).</description><identifier>ISSN: 0022-1899</identifier><identifier>EISSN: 1537-6613</identifier><identifier>DOI: 10.1086/314997</identifier><identifier>PMID: 10479136</identifier><identifier>CODEN: JIDIAQ</identifier><language>eng</language><publisher>Chicago, IL: The University of Chicago Press</publisher><subject>AIDS ; AIDS/HIV ; Alleles ; Biological and medical sciences ; Bisexuality ; Case-Control Studies ; CCR2b protein ; CCR5 protein ; Confidence Intervals ; Disease Progression ; DNA Primers ; Epidemiology ; Fundamental and applied biological sciences. Psychology ; Genetic mutation ; Genotype ; Genotypes ; HIV ; HIV 1 ; HIV Antibodies - blood ; HIV infections ; HIV Infections - genetics ; HIV Infections - immunology ; HIV Infections - physiopathology ; Homosexuality, Male ; Human immunodeficiency virus 1 ; Human viral diseases ; Humans ; Infections ; Infectious diseases ; Major Articles ; Male ; Medical sciences ; Microbiology ; Nucleotides ; Point Mutation ; Polymerase Chain Reaction ; Polymorphism, Genetic ; Prognosis ; Promoter Regions, Genetic ; Proportional Hazards Models ; Receptors, CCR2 ; Receptors, CCR5 - genetics ; Receptors, Chemokine - genetics ; Receptors, Cytokine - genetics ; SDF-1 protein ; Time Factors ; Viral diseases ; Viral diseases of the lymphoid tissue and the blood. Aids ; Virology</subject><ispartof>The Journal of infectious diseases, 1999-10, Vol.180 (4), p.1096-1105</ispartof><rights>Copyright 1999 Infectious Diseases Society of America</rights><rights>1999 INIST-CNRS</rights><rights>Copyright University of Chicago, acting through its Press Oct 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-bfb2bfccbf0a87893259262b9ec955743bb56cfc60a14ea57f3d7b7af3cbd2023</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/30109909$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/30109909$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,776,780,799,27901,27902,57992,58225</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1951658$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10479136$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Easterbrook, Philippa J.</creatorcontrib><creatorcontrib>Rostron, Tim</creatorcontrib><creatorcontrib>Ives, Natalie</creatorcontrib><creatorcontrib>Troop, Maxine</creatorcontrib><creatorcontrib>Gazzard, Brian G.</creatorcontrib><creatorcontrib>Rowland-Jones, Sarah L.</creatorcontrib><title>Chemokine Receptor Polymorphisms and Human Immunodeficiency Virus Disease Progression</title><title>The Journal of infectious diseases</title><addtitle>The Journal of Infectious Diseases</addtitle><description>The role of polymorphisms in genes encoding chemokines and their receptors (CCR2B, SDF-1, and the promoter region of CCR5) in human immunodeficiency virus (HIV) disease progression was studied in 132 white HIV type 1 (HlV-l)-infected participants from a United Kingdom cohort study. Genotyping was done by use of amplification refractory mutation system-polymerase chain reaction with sequence-specific primers, and Cox proportional hazards models were used to examine the impact of polymorphisms on time to a CD4 cell count <200 × 106/L and to CDC stage IV disease. The results confirm a significant association of the CCR2B-64I mutant genotype with slower progression to a CD4 count <200 (hazards ratio [HR], 0.39; 95% confidence interval [CI], 0.17–0.91) but not with the SDF-lα 3′ UTR homozygous mutation. The effects of the CCR5 and CCR2 mutations were genetically independent and similar in the magnitude of their protective effect on progression to a CD4 count <200 cells. A novel finding was an association of borderline significance between homozygosity for C at nucleotide position 59353 in the CCR5 promoter region and a slower rate of CD4 cell decline to <200 × 106/L (HR, 0.58; 95% CI, 0.34–0.996).</description><subject>AIDS</subject><subject>AIDS/HIV</subject><subject>Alleles</subject><subject>Biological and medical sciences</subject><subject>Bisexuality</subject><subject>Case-Control Studies</subject><subject>CCR2b protein</subject><subject>CCR5 protein</subject><subject>Confidence Intervals</subject><subject>Disease Progression</subject><subject>DNA Primers</subject><subject>Epidemiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetic mutation</subject><subject>Genotype</subject><subject>Genotypes</subject><subject>HIV</subject><subject>HIV 1</subject><subject>HIV Antibodies - blood</subject><subject>HIV infections</subject><subject>HIV Infections - genetics</subject><subject>HIV Infections - immunology</subject><subject>HIV Infections - physiopathology</subject><subject>Homosexuality, Male</subject><subject>Human immunodeficiency virus 1</subject><subject>Human viral diseases</subject><subject>Humans</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Major Articles</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microbiology</subject><subject>Nucleotides</subject><subject>Point Mutation</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Genetic</subject><subject>Prognosis</subject><subject>Promoter Regions, Genetic</subject><subject>Proportional Hazards Models</subject><subject>Receptors, CCR2</subject><subject>Receptors, CCR5 - genetics</subject><subject>Receptors, Chemokine - genetics</subject><subject>Receptors, Cytokine - genetics</subject><subject>SDF-1 protein</subject><subject>Time Factors</subject><subject>Viral diseases</subject><subject>Viral diseases of the lymphoid tissue and the blood. Aids</subject><subject>Virology</subject><issn>0022-1899</issn><issn>1537-6613</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0UFrFDEUB_Agil2rfgNlEPE2-pJMkslRttYtLFjFingJSSax2e5M1rwd6H57R2apxYunHP4_3iP_R8hzCm8ptPIdp43W6gFZUMFVLSXlD8kCgLGatlqfkCeIGwBouFSPyQmFRmnK5YJcLa9Dn2_SEKovwYfdPpfqMm8PfS6764Q9VnboqtXY26G66PtxyF2Iyacw-EP1LZURq7OEwWKoLkv-WQJiysNT8ijaLYZnx_eUXJ1_-Lpc1etPHy-W79e1b0Szr110zEXvXQTbqlZzJjSTzOngtRCq4c4J6aOXYGkTrFCRd8opG7l3HQPGT8mbee6u5F9jwL3pE_qw3doh5BGNmhqgYirjf5C2HCTjMMFX_8BNHsswfcIwxjVIfn-tLxmxhGh2JfW2HAwF8-ccZj7HBF8ep42uD909Nvc_gddHYNHbbSx28An_Oi2oFO3EXsxsg9OB7mIOFLQGPeX1nCfch9u73JYbIxVXwqy-_zBanMFnrdZmzX8Dh3mpmw</recordid><startdate>19991001</startdate><enddate>19991001</enddate><creator>Easterbrook, Philippa J.</creator><creator>Rostron, Tim</creator><creator>Ives, Natalie</creator><creator>Troop, Maxine</creator><creator>Gazzard, Brian G.</creator><creator>Rowland-Jones, Sarah L.</creator><general>The University of Chicago Press</general><general>University of Chicago Press</general><general>Oxford University Press</general><scope>BSCLL</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>K9.</scope><scope>NAPCQ</scope><scope>7U9</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19991001</creationdate><title>Chemokine Receptor Polymorphisms and Human Immunodeficiency Virus Disease Progression</title><author>Easterbrook, Philippa J. ; Rostron, Tim ; Ives, Natalie ; Troop, Maxine ; Gazzard, Brian G. ; Rowland-Jones, Sarah L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-bfb2bfccbf0a87893259262b9ec955743bb56cfc60a14ea57f3d7b7af3cbd2023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>AIDS</topic><topic>AIDS/HIV</topic><topic>Alleles</topic><topic>Biological and medical sciences</topic><topic>Bisexuality</topic><topic>Case-Control Studies</topic><topic>CCR2b protein</topic><topic>CCR5 protein</topic><topic>Confidence Intervals</topic><topic>Disease Progression</topic><topic>DNA Primers</topic><topic>Epidemiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetic mutation</topic><topic>Genotype</topic><topic>Genotypes</topic><topic>HIV</topic><topic>HIV 1</topic><topic>HIV Antibodies - blood</topic><topic>HIV infections</topic><topic>HIV Infections - genetics</topic><topic>HIV Infections - immunology</topic><topic>HIV Infections - physiopathology</topic><topic>Homosexuality, Male</topic><topic>Human immunodeficiency virus 1</topic><topic>Human viral diseases</topic><topic>Humans</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Major Articles</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Microbiology</topic><topic>Nucleotides</topic><topic>Point Mutation</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Genetic</topic><topic>Prognosis</topic><topic>Promoter Regions, Genetic</topic><topic>Proportional Hazards Models</topic><topic>Receptors, CCR2</topic><topic>Receptors, CCR5 - genetics</topic><topic>Receptors, Chemokine - genetics</topic><topic>Receptors, Cytokine - genetics</topic><topic>SDF-1 protein</topic><topic>Time Factors</topic><topic>Viral diseases</topic><topic>Viral diseases of the lymphoid tissue and the blood. Aids</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Easterbrook, Philippa J.</creatorcontrib><creatorcontrib>Rostron, Tim</creatorcontrib><creatorcontrib>Ives, Natalie</creatorcontrib><creatorcontrib>Troop, Maxine</creatorcontrib><creatorcontrib>Gazzard, Brian G.</creatorcontrib><creatorcontrib>Rowland-Jones, Sarah L.</creatorcontrib><collection>Istex</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of infectious diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Easterbrook, Philippa J.</au><au>Rostron, Tim</au><au>Ives, Natalie</au><au>Troop, Maxine</au><au>Gazzard, Brian G.</au><au>Rowland-Jones, Sarah L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Chemokine Receptor Polymorphisms and Human Immunodeficiency Virus Disease Progression</atitle><jtitle>The Journal of infectious diseases</jtitle><addtitle>The Journal of Infectious Diseases</addtitle><date>1999-10-01</date><risdate>1999</risdate><volume>180</volume><issue>4</issue><spage>1096</spage><epage>1105</epage><pages>1096-1105</pages><issn>0022-1899</issn><eissn>1537-6613</eissn><coden>JIDIAQ</coden><abstract>The role of polymorphisms in genes encoding chemokines and their receptors (CCR2B, SDF-1, and the promoter region of CCR5) in human immunodeficiency virus (HIV) disease progression was studied in 132 white HIV type 1 (HlV-l)-infected participants from a United Kingdom cohort study. Genotyping was done by use of amplification refractory mutation system-polymerase chain reaction with sequence-specific primers, and Cox proportional hazards models were used to examine the impact of polymorphisms on time to a CD4 cell count <200 × 106/L and to CDC stage IV disease. The results confirm a significant association of the CCR2B-64I mutant genotype with slower progression to a CD4 count <200 (hazards ratio [HR], 0.39; 95% confidence interval [CI], 0.17–0.91) but not with the SDF-lα 3′ UTR homozygous mutation. The effects of the CCR5 and CCR2 mutations were genetically independent and similar in the magnitude of their protective effect on progression to a CD4 count <200 cells. A novel finding was an association of borderline significance between homozygosity for C at nucleotide position 59353 in the CCR5 promoter region and a slower rate of CD4 cell decline to <200 × 106/L (HR, 0.58; 95% CI, 0.34–0.996).</abstract><cop>Chicago, IL</cop><pub>The University of Chicago Press</pub><pmid>10479136</pmid><doi>10.1086/314997</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | The Journal of infectious diseases, 1999-10, Vol.180 (4), p.1096-1105 |
| issn | 0022-1899 1537-6613 |
| language | eng |
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| source | Jstor Complete Legacy; Oxford University Press Journals All Titles (1996-Current); MEDLINE |
| subjects | AIDS AIDS/HIV Alleles Biological and medical sciences Bisexuality Case-Control Studies CCR2b protein CCR5 protein Confidence Intervals Disease Progression DNA Primers Epidemiology Fundamental and applied biological sciences. Psychology Genetic mutation Genotype Genotypes HIV HIV 1 HIV Antibodies - blood HIV infections HIV Infections - genetics HIV Infections - immunology HIV Infections - physiopathology Homosexuality, Male Human immunodeficiency virus 1 Human viral diseases Humans Infections Infectious diseases Major Articles Male Medical sciences Microbiology Nucleotides Point Mutation Polymerase Chain Reaction Polymorphism, Genetic Prognosis Promoter Regions, Genetic Proportional Hazards Models Receptors, CCR2 Receptors, CCR5 - genetics Receptors, Chemokine - genetics Receptors, Cytokine - genetics SDF-1 protein Time Factors Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids Virology |
| title | Chemokine Receptor Polymorphisms and Human Immunodeficiency Virus Disease Progression |
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