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Article: Role of polymorphisms of the inflammatory response genes and DC-SIGNR in genetic susceptibility to SARS and other infections.
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TitleRole of polymorphisms of the inflammatory response genes and DC-SIGNR in genetic susceptibility to SARS and other infections.
 
AuthorsKhoo, US2
Chan, KY2
Chan, VS2
Ching, JC
Yam, L
Chu, CM
Lai, ST
Wong, TY
Tam, P4
Yip, SP5
Leung, GM3
Lin, CL1
Peiris, JS6
 
Issue Date2008
 
PublisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.org/resources/supp.html
 
CitationHong Kong Medical Journal, 2008, v. 14 suppl. 4, p. 31-35 [How to Cite?]
 
Abstract1. A genetic risk-association study involving more than 1200 subjects showed individuals homozygous for L-SIGN tandem repeats are less susceptible to SARS infection. 2. This was supported by in vitro binding studies that demonstrated homozygous L-SIGN, compared to heterozygous, had higher binding capacity for SARS coronavirus (SARS-CoV), with higher proteasome-dependent viral degradation. In contrast, homozygous L-SIGN demonstrated lower binding capacity for HIV1-gp120.3. Genetic-association studies for single nucleotide polymorphisms of the inflammatory response genes, namely TNF-alpha, INF-alpha, INF-beta, INF-gamma, IL1-alpha, IL1-beta, IL-4, IL-6 and iNOS, failed to show a significant association with SARS clinical outcomes or susceptibility.
 
DescriptionResearch Fund for the Control of Infectious Diseases: Research Dissemination Reports (Series 2)
 
ISSN1024-2708
2013 SCImago Journal Rankings: 0.293
 
DC FieldValue
dc.contributor.authorKhoo, US
 
dc.contributor.authorChan, KY
 
dc.contributor.authorChan, VS
 
dc.contributor.authorChing, JC
 
dc.contributor.authorYam, L
 
dc.contributor.authorChu, CM
 
dc.contributor.authorLai, ST
 
dc.contributor.authorWong, TY
 
dc.contributor.authorTam, P
 
dc.contributor.authorYip, SP
 
dc.contributor.authorLeung, GM
 
dc.contributor.authorLin, CL
 
dc.contributor.authorPeiris, JS
 
dc.date.accessioned2010-04-12T01:34:18Z
 
dc.date.available2010-04-12T01:34:18Z
 
dc.date.issued2008
 
dc.description.abstract1. A genetic risk-association study involving more than 1200 subjects showed individuals homozygous for L-SIGN tandem repeats are less susceptible to SARS infection. 2. This was supported by in vitro binding studies that demonstrated homozygous L-SIGN, compared to heterozygous, had higher binding capacity for SARS coronavirus (SARS-CoV), with higher proteasome-dependent viral degradation. In contrast, homozygous L-SIGN demonstrated lower binding capacity for HIV1-gp120.3. Genetic-association studies for single nucleotide polymorphisms of the inflammatory response genes, namely TNF-alpha, INF-alpha, INF-beta, INF-gamma, IL1-alpha, IL1-beta, IL-4, IL-6 and iNOS, failed to show a significant association with SARS clinical outcomes or susceptibility.
 
dc.description.naturepublished_or_final_version
 
dc.descriptionResearch Fund for the Control of Infectious Diseases: Research Dissemination Reports (Series 2)
 
dc.identifier.citationHong Kong Medical Journal, 2008, v. 14 suppl. 4, p. 31-35 [How to Cite?]
 
dc.identifier.epage35
 
dc.identifier.hkuros150914
 
dc.identifier.issn1024-2708
2013 SCImago Journal Rankings: 0.293
 
dc.identifier.issuesuppl. 4
 
dc.identifier.openurl
 
dc.identifier.pmid18708672
 
dc.identifier.scopuseid_2-s2.0-70449903273
 
dc.identifier.spage31
 
dc.identifier.urihttp://hdl.handle.net/10722/57361
 
dc.identifier.volume14
 
dc.languageeng
 
dc.publisherHong Kong Medical Association. The Journal's web site is located at http://www.hkmj.org/resources/supp.html
 
dc.publisher.placeHong Kong
 
dc.relation.ispartofHong Kong Medical Journal
 
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Medical Association.
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshAdult
 
dc.subject.meshAlleles
 
dc.subject.meshAnalysis of Variance
 
dc.subject.meshCase-Control Studies
 
dc.subject.meshCell Adhesion Molecules - genetics
 
dc.subject.meshCommunicable Diseases - genetics - physiopathology
 
dc.subject.meshConfidence Intervals
 
dc.subject.meshCytokines - genetics - metabolism
 
dc.subject.meshFemale
 
dc.subject.meshGene Frequency
 
dc.subject.meshGenetic Predisposition to Disease
 
dc.subject.meshHumans
 
dc.subject.meshLectins, C-Type - genetics
 
dc.subject.meshMale
 
dc.subject.meshMiddle Aged
 
dc.subject.meshOdds Ratio
 
dc.subject.meshPolymorphism, Genetic
 
dc.subject.meshProbability
 
dc.subject.meshReceptors, Cell Surface - genetics
 
dc.subject.meshSARS Virus - genetics - metabolism
 
dc.subject.meshSevere Acute Respiratory Syndrome - genetics - physiopathology
 
dc.subject.meshTandem Repeat Sequences
 
dc.subject.meshTumor Necrosis Factor-alpha - genetics - metabolism
 
dc.titleRole of polymorphisms of the inflammatory response genes and DC-SIGNR in genetic susceptibility to SARS and other infections.
 
dc.typeArticle
 
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<contributor.author>Chu, CM</contributor.author>
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<contributor.author>Wong, TY</contributor.author>
<contributor.author>Tam, P</contributor.author>
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<description.abstract>1. A genetic risk-association study involving more than 1200 subjects showed individuals homozygous for L-SIGN tandem repeats are less susceptible to SARS infection. 2. This was supported by in vitro binding studies that demonstrated homozygous L-SIGN, compared to heterozygous, had higher binding capacity for SARS coronavirus (SARS-CoV), with higher proteasome-dependent viral degradation. In contrast, homozygous L-SIGN demonstrated lower binding capacity for HIV1-gp120.3. Genetic-association studies for single nucleotide polymorphisms of the inflammatory response genes, namely TNF-alpha, INF-alpha, INF-beta, INF-gamma, IL1-alpha, IL1-beta, IL-4, IL-6 and iNOS, failed to show a significant association with SARS clinical outcomes or susceptibility.</description.abstract>
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<subject.mesh>Adult</subject.mesh>
<subject.mesh>Alleles</subject.mesh>
<subject.mesh>Analysis of Variance</subject.mesh>
<subject.mesh>Case-Control Studies</subject.mesh>
<subject.mesh>Cell Adhesion Molecules - genetics</subject.mesh>
<subject.mesh>Communicable Diseases - genetics - physiopathology</subject.mesh>
<subject.mesh>Confidence Intervals</subject.mesh>
<subject.mesh>Cytokines - genetics - metabolism</subject.mesh>
<subject.mesh>Female</subject.mesh>
<subject.mesh>Gene Frequency</subject.mesh>
<subject.mesh>Genetic Predisposition to Disease</subject.mesh>
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<subject.mesh>Lectins, C-Type - genetics</subject.mesh>
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<subject.mesh>Middle Aged</subject.mesh>
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Author Affiliations
  1. Centre for Health Protection
  2. The University of Hong Kong
  3. Princess Margaret Hospital Hong Kong
  4. Pamela Youde Nethersole Eastern Hospital
  5. United Christian Hospital Hong Kong
  6. Hong Kong Polytechnic University