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Article: Association of ICAM3 genetic variant with severe acute respiratory syndrome

TitleAssociation of ICAM3 genetic variant with severe acute respiratory syndrome
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.org
Citation
Journal Of Infectious Diseases, 2007, v. 196 n. 2, p. 271-280 How to Cite?
AbstractGenetic polymorphisms have been demonstrated to be associated with vulnerability to human infection. ICAM3, an intercellular adhesion molecule important for T cell activation, and FCER2 (CD23), an immune response gene, both located on chromosome 19p13.3, were investigated for host genetic susceptibility and association with clinical outcome. A case-control study based on 817 patients with confirmed severe acute respiratory syndrome (SARS), 307 health care worker control subjects, 290 outpatient control subjects, and 309 household control subjects unaffected by SARS from Hong Kong was conducted to test for genetic association. No significant association to susceptibility to SARS infection caused by the novel coronavirus (SARS-CoV) was found for the FCER2 and the ICAM3 single nucleotide polymorphisms. However, patients with SARS homozygous for ICAM3 Gly143 showed significant association with higher lactate dehydrogenase levels (P = .0067; odds ratio [OR], 4.31 [95% confidence interval {CI}, 1.37-13.56]) and lower total white blood cell counts (P = .022; OR, 0.30 [95% CI, 0.10-0.89]) on admission. These findings support the role of ICAM3 in the immunopathogenesis of SARS. © 2007 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/57176
ISSN
2015 Impact Factor: 6.344
2015 SCImago Journal Rankings: 4.000
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorChing, JCYen_HK
dc.contributor.authorXu, MSen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorYip, SPen_HK
dc.contributor.authorYam, LYCen_HK
dc.contributor.authorLai, STen_HK
dc.contributor.authorChu, CMen_HK
dc.contributor.authorWong, ATYen_HK
dc.contributor.authorSong, YQen_HK
dc.contributor.authorHuang, FPen_HK
dc.contributor.authorLiu, Wen_HK
dc.contributor.authorChung, PHen_HK
dc.contributor.authorLeung, GMen_HK
dc.contributor.authorChow, EYDen_HK
dc.contributor.authorChan, EYTen_HK
dc.contributor.authorChan, JCKen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorTam, Pen_HK
dc.contributor.authorChan, LCen_HK
dc.contributor.authorSham, Pen_HK
dc.contributor.authorChan, VSFen_HK
dc.contributor.authorPeiris, Men_HK
dc.contributor.authorLin, SCLen_HK
dc.contributor.authorKhoo, USen_HK
dc.date.accessioned2010-04-12T01:28:21Z-
dc.date.available2010-04-12T01:28:21Z-
dc.date.issued2007en_HK
dc.identifier.citationJournal Of Infectious Diseases, 2007, v. 196 n. 2, p. 271-280en_HK
dc.identifier.issn0022-1899en_HK
dc.identifier.urihttp://hdl.handle.net/10722/57176-
dc.description.abstractGenetic polymorphisms have been demonstrated to be associated with vulnerability to human infection. ICAM3, an intercellular adhesion molecule important for T cell activation, and FCER2 (CD23), an immune response gene, both located on chromosome 19p13.3, were investigated for host genetic susceptibility and association with clinical outcome. A case-control study based on 817 patients with confirmed severe acute respiratory syndrome (SARS), 307 health care worker control subjects, 290 outpatient control subjects, and 309 household control subjects unaffected by SARS from Hong Kong was conducted to test for genetic association. No significant association to susceptibility to SARS infection caused by the novel coronavirus (SARS-CoV) was found for the FCER2 and the ICAM3 single nucleotide polymorphisms. However, patients with SARS homozygous for ICAM3 Gly143 showed significant association with higher lactate dehydrogenase levels (P = .0067; odds ratio [OR], 4.31 [95% confidence interval {CI}, 1.37-13.56]) and lower total white blood cell counts (P = .022; OR, 0.30 [95% CI, 0.10-0.89]) on admission. These findings support the role of ICAM3 in the immunopathogenesis of SARS. © 2007 by the Infectious Diseases Society of America. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://jid.oxfordjournals.orgen_HK
dc.relation.ispartofJournal of Infectious Diseasesen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAntigens, CD - geneticsen_HK
dc.subject.meshCell Adhesion Molecules - geneticsen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshL-Lactate Dehydrogenase - blooden_HK
dc.subject.meshPolymorphism, Single Nucleotide - geneticsen_HK
dc.titleAssociation of ICAM3 genetic variant with severe acute respiratory syndromeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1899&volume=196&issue=2&spage=271&epage=280&date=2007&atitle=Association+of+ICAM3+genetic+variant+with+severe+acute+respiratory+syndromeen_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailSong, YQ: songy@hku.hken_HK
dc.identifier.emailLeung, GM: gmleung@hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailTam, P: paultam@hku.hken_HK
dc.identifier.emailChan, LC: chanlc@hkucc.hku.hken_HK
dc.identifier.emailSham, P: pcsham@hku.hken_HK
dc.identifier.emailChan, VSF: sfvchan@hku.hken_HK
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authoritySong, YQ=rp00488en_HK
dc.identifier.authorityLeung, GM=rp00460en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityTam, P=rp00060en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.identifier.authoritySham, P=rp00459en_HK
dc.identifier.authorityChan, VSF=rp01459en_HK
dc.identifier.authorityPeiris, M=rp00410en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1086/518892en_HK
dc.identifier.pmid17570115-
dc.identifier.scopuseid_2-s2.0-34447292078en_HK
dc.identifier.hkuros129150-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34447292078&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume196en_HK
dc.identifier.issue2en_HK
dc.identifier.spage271en_HK
dc.identifier.epage280en_HK
dc.identifier.isiWOS:000247803100015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridChing, JCY=15735635300en_HK
dc.identifier.scopusauthoridXu, MS=35957113100en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridYip, SP=7102133673en_HK
dc.identifier.scopusauthoridYam, LYC=7102764741en_HK
dc.identifier.scopusauthoridLai, ST=7402937038en_HK
dc.identifier.scopusauthoridChu, CM=7404345558en_HK
dc.identifier.scopusauthoridWong, ATY=36921624400en_HK
dc.identifier.scopusauthoridSong, YQ=7404921212en_HK
dc.identifier.scopusauthoridHuang, FP=35358818300en_HK
dc.identifier.scopusauthoridLiu, W=36078432200en_HK
dc.identifier.scopusauthoridChung, PH=34568741300en_HK
dc.identifier.scopusauthoridLeung, GM=7007159841en_HK
dc.identifier.scopusauthoridChow, EYD=7102595571en_HK
dc.identifier.scopusauthoridChan, EYT=7401994013en_HK
dc.identifier.scopusauthoridChan, JCK=23090202000en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridTam, P=7202539421en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK
dc.identifier.scopusauthoridSham, P=34573429300en_HK
dc.identifier.scopusauthoridChan, VSF=35200370000en_HK
dc.identifier.scopusauthoridPeiris, M=7005486823en_HK
dc.identifier.scopusauthoridLin, SCL=36475190600en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK

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