Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals
Identifieur interne : 000585 ( Istex/Corpus ); précédent : 000584; suivant : 000586Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals
Auteurs : Anurag Rathore ; Animesh Chatterjee ; P. Sivarama ; Naohiko Yamamoto ; Tapan N. DholeSource :
- Journal of Clinical Immunology [ 0271-9142 ] ; 2008-01-01.
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- KwdEn :
Abstract
Abstract: Despite multiple sexual exposures to HIV-1 virus, some individuals remain HIV-1 seronegative. Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell in trans, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (n = 47) individuals, HIV-1 seronegative (n = 262) healthy control, and HIV-1-infected seropositive patients (n = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or χ 2 test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (p = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.
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DOI: 10.1007/s10875-007-9131-x
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Sivarama</name><affiliation><mods:affiliation>AIDS Counseling and Treatment Center, Belgaum, India</mods:affiliation></affiliation></author><author><name sortKey="Yamamoto, Naohiko" sort="Yamamoto, Naohiko" uniqKey="Yamamoto N" first="Naohiko" last="Yamamoto">Naohiko Yamamoto</name><affiliation><mods:affiliation>Department of International Health, Nagoya University School of Medicine, Nagoya, Japan</mods:affiliation></affiliation></author><author><name sortKey="Dhole, Tapan N" sort="Dhole, Tapan N" uniqKey="Dhole T" first="Tapan N." last="Dhole">Tapan N. Dhole</name><affiliation><mods:affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: tndhole@hotmail.com</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Clinical Immunology</title><title level="j" type="abbrev">J Clin Immunol</title><idno type="ISSN">0271-9142</idno><idno type="eISSN">1573-2592</idno><imprint><publisher>Springer US; http://www.springer-ny.com</publisher><pubPlace>Boston</pubPlace><date type="published" when="2008-01-01">2008-01-01</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="50">50</biblScope><biblScope unit="page" to="57">57</biblScope></imprint><idno type="ISSN">0271-9142</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0271-9142</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DC-SIGN</term><term>DC-SIGNR</term><term>HIV-1</term><term>gene polymorphism</term><term>genetic association</term><term>tandem repeats</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Despite multiple sexual exposures to HIV-1 virus, some individuals remain HIV-1 seronegative. Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell in trans, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (n = 47) individuals, HIV-1 seronegative (n = 262) healthy control, and HIV-1-infected seropositive patients (n = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or χ 2 test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (p = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.</div></front></TEI><istex><corpusName>springer-journals</corpusName><author><json:item><name>Anurag Rathore</name><affiliations><json:string>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</json:string></affiliations></json:item><json:item><name>Animesh Chatterjee</name><affiliations><json:string>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</json:string></affiliations></json:item><json:item><name>P. Sivarama</name><affiliations><json:string>AIDS Counseling and Treatment Center, Belgaum, India</json:string></affiliations></json:item><json:item><name>Naohiko Yamamoto</name><affiliations><json:string>Department of International Health, Nagoya University School of Medicine, Nagoya, Japan</json:string></affiliations></json:item><json:item><name>Tapan N. 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Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell in trans, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (n = 47) individuals, HIV-1 seronegative (n = 262) healthy control, and HIV-1-infected seropositive patients (n = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or χ 2 test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (p = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.</abstract><qualityIndicators><score>9.06</score><pdfWordCount>4060</pdfWordCount><pdfCharCount>27082</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>8</pdfPageCount><pdfPageSize>595.276 x 790.866 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractWordCount>255</abstractWordCount><abstractCharCount>1824</abstractCharCount><keywordCount>6</keywordCount></qualityIndicators><title>Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals</title><genre><json:string>research-article</json:string></genre><host><title>Journal of Clinical Immunology</title><language><json:string>unknown</json:string></language><publicationDate>2008</publicationDate><copyrightDate>2008</copyrightDate><issn><json:string>0271-9142</json:string></issn><eissn><json:string>1573-2592</json:string></eissn><journalId><json:string>10875</json:string></journalId><volume>28</volume><issue>1</issue><pages><first>50</first><last>57</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Medical Microbiology</value></json:item><json:item><value>Internal Medicine</value></json:item><json:item><value>Infectious Diseases</value></json:item><json:item><value>Immunology</value></json:item></subject></host><ark><json:string>ark:/67375/VQC-M6TN1N0C-H</json:string></ark><publicationDate>2008</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1007/s10875-007-9131-x</json:string></doi><id>9F928F739F1DB91A3396D803975A9B39B2F90D7A</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-M6TN1N0C-H/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-M6TN1N0C-H/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/VQC-M6TN1N0C-H/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Springer US; 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http://www.springer-ny.com</publisher><pubPlace>Boston</pubPlace><date type="published" when="2008-01-01"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="50">50</biblScope><biblScope unit="page" to="57">57</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007-06-16</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Abstract: Despite multiple sexual exposures to HIV-1 virus, some individuals remain HIV-1 seronegative. Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell in trans, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (n = 47) individuals, HIV-1 seronegative (n = 262) healthy control, and HIV-1-infected seropositive patients (n = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or χ 2 test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (p = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>DC-SIGN</term></item><item><term>DC-SIGNR</term></item><item><term>HIV-1</term></item><item><term>tandem repeats</term></item><item><term>genetic association</term></item><item><term>gene polymorphism</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Biomedicine</head><item><term>Medical Microbiology</term></item><item><term>Internal Medicine</term></item><item><term>Infectious Diseases</term></item><item><term>Immunology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-06-16">Created</change><change 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TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd><IssueArticleCount>16</IssueArticleCount><IssueHistory><OnlineDate><Year>2008</Year><Month>1</Month><Day>9</Day></OnlineDate><PrintDate><Year>2008</Year><Month>1</Month><Day>9</Day></PrintDate><CoverDate><Year>2008</Year><Month>1</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer Science+Business Media, LLC</CopyrightHolderName><CopyrightYear>2008</CopyrightYear></IssueCopyright></IssueInfo><Article ID="s10875-007-9131-x" OutputMedium="All"><ArticleInfo ArticleType="OriginalPaper" ContainsESM="No" Language="En" NumberingStyle="Unnumbered" TocLevels="0"><ArticleID>9131</ArticleID><ArticleDOI>10.1007/s10875-007-9131-x</ArticleDOI><ArticleSequenceNumber>8</ArticleSequenceNumber><ArticleTitle Language="En">Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals</ArticleTitle><ArticleFirstPage>50</ArticleFirstPage><ArticleLastPage>57</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2007</Year><Month>8</Month><Day>21</Day></RegistrationDate><Received><Year>2007</Year><Month>6</Month><Day>16</Day></Received><Accepted><Year>2007</Year><Month>8</Month><Day>21</Day></Accepted><OnlineDate><Year>2007</Year><Month>9</Month><Day>18</Day></OnlineDate></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer Science+Business Media, LLC</CopyrightHolderName><CopyrightYear>2007</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Anurag</GivenName><FamilyName>Rathore</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Animesh</GivenName><FamilyName>Chatterjee</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff2"><AuthorName DisplayOrder="Western"><GivenName>P.</GivenName><FamilyName>Sivarama</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff3"><AuthorName DisplayOrder="Western"><GivenName>Naohiko</GivenName><FamilyName>Yamamoto</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1" CorrespondingAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Tapan</GivenName><GivenName>N.</GivenName><FamilyName>Dhole</FamilyName></AuthorName><Contact><Phone>+91-522-2668100</Phone><Fax>+91-522-2668100</Fax><Email>tndhole@hotmail.com</Email></Contact></Author><Affiliation ID="Aff1"><OrgDivision>Department of Microbiology</OrgDivision><OrgName>Sanjay Gandhi Post Graduate Institute of Medical Sciences</OrgName><OrgAddress><Street>Raebarelli Road</Street><City>Lucknow</City><Postcode>226014</Postcode><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff2"><OrgName>AIDS Counseling and Treatment Center</OrgName><OrgAddress><City>Belgaum</City><Country Code="IN">India</Country></OrgAddress></Affiliation><Affiliation ID="Aff3"><OrgDivision>Department of International Health</OrgDivision><OrgName>Nagoya University School of Medicine</OrgName><OrgAddress><City>Nagoya</City><Country Code="JP">Japan</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Abstract</Heading><Para>Despite multiple sexual exposures to HIV-1 virus, some individuals remain HIV-1 seronegative. Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell <Emphasis Type="Italic">in trans</Emphasis>, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (<Emphasis Type="Italic">n</Emphasis> = 47) individuals, HIV-1 seronegative (<Emphasis Type="Italic">n</Emphasis> = 262) healthy control, and HIV-1-infected seropositive patients (<Emphasis Type="Italic">n</Emphasis> = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or <Emphasis Type="Italic">χ</Emphasis><Superscript>2</Superscript> test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (<Emphasis Type="Italic">p</Emphasis> = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>DC-SIGN</Keyword><Keyword>DC-SIGNR</Keyword><Keyword>HIV-1</Keyword><Keyword>tandem repeats</Keyword><Keyword>genetic association</Keyword><Keyword>gene polymorphism</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Role of Homozygous DC-SIGNR 5/5 Tandem Repeat Polymorphism in HIV-1 Exposed Seronegative North Indian Individuals</title></titleInfo><name type="personal"><namePart type="given">Anurag</namePart><namePart type="family">Rathore</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Animesh</namePart><namePart type="family">Chatterjee</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Sivarama</namePart><affiliation>AIDS Counseling and Treatment Center, Belgaum, India</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naohiko</namePart><namePart type="family">Yamamoto</namePart><affiliation>Department of International Health, Nagoya University School of Medicine, Nagoya, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal" displayLabel="corresp"><namePart type="given">Tapan</namePart><namePart type="given">N.</namePart><namePart type="family">Dhole</namePart><affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</affiliation><affiliation>E-mail: tndhole@hotmail.com</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>Springer US; http://www.springer-ny.com</publisher><place><placeTerm type="text">Boston</placeTerm></place><dateCreated encoding="w3cdtf">2007-06-16</dateCreated><dateIssued encoding="w3cdtf">2008-01-01</dateIssued><copyrightDate encoding="w3cdtf">2007</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract lang="en">Abstract: Despite multiple sexual exposures to HIV-1 virus, some individuals remain HIV-1 seronegative. Although several genetic factors have been related to HIV-1 resistance, the homozygosity for a mutation in CCR5 gene (the 32-bp deletion, i.e., CCR5-Delta32 allele) is presently considered the most relevant one. The C-type lectins, DC-SIGN (present on dendritic cells and macrophages) and DC-SIGNR (present on endothelial cells in liver and lymph nodes) efficiently bind and transmit HIV-1 to susceptible cell in trans, thereby augmenting the infection. A potential association of the DC-SIGN and DC-SIGNR neck domain repeat polymorphism and risk of HIV-1 infection is currently under debate. To determine the influence of host genetic factors on HIV-1 resistance, we conducted genetic risk association study in HIV-1-exposed seronegative (n = 47) individuals, HIV-1 seronegative (n = 262) healthy control, and HIV-1-infected seropositive patients (n = 168) for polymorphism in neck domain of DC-SIGN and DC-SIGNR genes. The DC-SIGN and DC-SIGNR genotypes were identified by polymerase chain reaction method in DNA extracted from peripheral blood and confirmed by sequencing. Fisher exact or χ 2 test was used for static analysis. DC-SIGN genotype and allele distribution was fairly similar in HIV-1-exposed seronegative, HIV-1 seropositive, and HIV-1 seronegative control. There was no statistical significance in the differences in the distribution of DC-SIGN genotypes. A total of 13 genotypes were found in DC-SIGNR neck repeat region polymorphism. Among all the genotypes, only 5/5 homozygous showed significant reduced risk of HIV-1 infection in HIV-1-exposed seronegative individuals (p = 0.009). A unique genotype 8/5 heterozygous was also found in HIV-1 seropositive individual, which is not reported elsewhere.</abstract><subject lang="en"><genre>Keywords</genre><topic>DC-SIGN</topic><topic>DC-SIGNR</topic><topic>HIV-1</topic><topic>tandem repeats</topic><topic>genetic association</topic><topic>gene polymorphism</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Clinical Immunology</title></titleInfo><titleInfo type="abbreviated"><title>J Clin Immunol</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>Springer</publisher><dateIssued encoding="w3cdtf">2008-01-09</dateIssued><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><subject><genre>Biomedicine</genre><topic>Medical Microbiology</topic><topic>Internal Medicine</topic><topic>Infectious Diseases</topic><topic>Immunology</topic></subject><identifier type="ISSN">0271-9142</identifier><identifier type="eISSN">1573-2592</identifier><identifier type="JournalID">10875</identifier><identifier type="IssueArticleCount">16</identifier><identifier type="VolumeIssueCount">6</identifier><part><date>2008</date><detail type="volume"><number>28</number><caption>vol.</caption></detail><detail type="issue"><number>1</number><caption>no.</caption></detail><extent unit="pages"><start>50</start><end>57</end></extent></part><recordInfo><recordOrigin>Springer Science+Business Media, LLC, 2008</recordOrigin></recordInfo></relatedItem><identifier type="istex">9F928F739F1DB91A3396D803975A9B39B2F90D7A</identifier><identifier type="ark">ark:/67375/VQC-M6TN1N0C-H</identifier><identifier type="DOI">10.1007/s10875-007-9131-x</identifier><identifier type="ArticleID">9131</identifier><identifier type="ArticleID">s10875-007-9131-x</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer Science+Business Media, LLC, 2007</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-3XSW68JL-F">springer</recordContentSource><recordOrigin>Springer Science+Business Media, LLC, 2007</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/VQC-M6TN1N0C-H/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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