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.
English descriptors
- 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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<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>
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<ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>Anurag</GivenName>
<FamilyName>Rathore</FamilyName>
</AuthorName>
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<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>
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<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>
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<NoBody></NoBody>
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<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>
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<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>
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<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>
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<name type="personal"><namePart type="given">Animesh</namePart>
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<affiliation>Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarelli Road, 226014, Lucknow, India</affiliation>
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<name type="personal"><namePart type="given">P.</namePart>
<namePart type="family">Sivarama</namePart>
<affiliation>AIDS Counseling and Treatment Center, Belgaum, India</affiliation>
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<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>
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<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>
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<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>
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<relatedItem type="host"><titleInfo><title>Journal of Clinical Immunology</title>
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<dateIssued encoding="w3cdtf">2008-01-09</dateIssued>
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<subject><genre>Biomedicine</genre>
<topic>Medical Microbiology</topic>
<topic>Internal Medicine</topic>
<topic>Infectious Diseases</topic>
<topic>Immunology</topic>
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<identifier type="ISSN">0271-9142</identifier>
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