Article: Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection

TitleHomozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
Authors
KeywordsSpecies Index: Animalia
Coronavirus
Sars Coronavirus
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com
Citation
Nature Genetics, 2006, v. 38 n. 1, p. 38-46 How to Cite?
Abstract
Severe acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection. © 2006 Nature Publishing Group.
Persistent Identifierhttp://hdl.handle.net/10722/132497
ISSN
2013 Impact Factor: 29.648
2013 SCImago Journal Rankings: 24.052
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. Nuffield Department of Clinical Medicine
  3. Imperial College London
  4. Weatherall Institute of Molecular Medicine
  5. Hong Kong Polytechnic University
DC FieldValueLanguage
dc.contributor.authorChan, VSFen_HK
dc.contributor.authorChan, KYKen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorPoon, LLMen_HK
dc.contributor.authorCheung, ANYen_HK
dc.contributor.authorZheng, Ben_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorMak, Wen_HK
dc.contributor.authorNgan, HYSen_HK
dc.contributor.authorXu, Xen_HK
dc.contributor.authorScreaton, Gen_HK
dc.contributor.authorTam, PKHen_HK
dc.contributor.authorAustyn, JMen_HK
dc.contributor.authorChan, LCen_HK
dc.contributor.authorYip, SPen_HK
dc.contributor.authorPeiris, Men_HK
dc.contributor.authorKhoo, USen_HK
dc.contributor.authorLin, CLSen_HK
dc.date.accessioned2011-03-28T09:25:26Z-
dc.date.available2011-03-28T09:25:26Z-
dc.date.issued2006en_HK
dc.identifier.citationNature Genetics, 2006, v. 38 n. 1, p. 38-46en_HK
dc.identifier.issn1061-4036en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132497-
dc.description.abstractSevere acute respiratory syndrome (SARS) is caused by infection of a previously undescribed coronavirus (CoV). L-SIGN, encoded by CLEC4M (also known as CD209L), is a SARS-CoV binding receptor that has polymorphism in its extracellular neck region encoded by the tandem repeat domain in exon 4. Our genetic risk association study shows that individuals homozygous for CLEC4M tandem repeats are less susceptible to SARS infection. L-SIGN is expressed in both non-SARS and SARS-CoV-infected lung. Compared with cells heterozygous for L-SIGN, cells homozygous for L-SIGN show higher binding capacity for SARS-CoV, higher proteasome-dependent viral degradation and a lower capacity for trans infection. Thus, homozygosity for L-SIGN plays a protective role during SARS infection. © 2006 Nature Publishing Group.en_HK
dc.languageengen_US
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.genetics.nature.comen_HK
dc.relation.ispartofNature Geneticsen_HK
dc.subjectSpecies Index: Animaliaen_US
dc.subjectCoronavirusen_US
dc.subjectSars Coronavirusen_US
dc.subject.meshAnimalsen_HK
dc.subject.meshCHO Cells - virologyen_HK
dc.subject.meshCell Adhesion Molecules - genetics - metabolismen_HK
dc.subject.meshCercopithecus aethiopsen_HK
dc.subject.meshCohort Studiesen_HK
dc.subject.meshCricetinaeen_HK
dc.subject.meshCricetulusen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHomozygoteen_HK
dc.subject.meshHong Kong - epidemiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntestine, Small - physiologyen_HK
dc.subject.meshLectins, C-Type - genetics - metabolismen_HK
dc.subject.meshLung - physiology - virologyen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshProteasome Endopeptidase Complex - metabolismen_HK
dc.subject.meshReceptors, Cell Surface - genetics - metabolismen_HK
dc.subject.meshSARS Virus - metabolism - pathogenicityen_HK
dc.subject.meshSevere Acute Respiratory Syndrome - epidemiology - geneticsen_HK
dc.subject.meshTandem Repeat Sequencesen_HK
dc.subject.meshVero Cells - virologyen_HK
dc.titleHomozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infectionen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, VSF: sfvchan@hku.hken_HK
dc.identifier.emailChan, KYK: kelvinc@pathology.hku.hken_HK
dc.identifier.emailPoon, LLM: llmpoon@hkucc.hku.hken_HK
dc.identifier.emailCheung, ANY: anycheun@hkucc.hku.hken_HK
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hken_HK
dc.identifier.emailNgan, HYS: hysngan@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hku.hken_HK
dc.identifier.emailChan, LC: chanlc@hkucc.hku.hken_HK
dc.identifier.emailPeiris, M: malik@hkucc.hku.hken_HK
dc.identifier.emailKhoo, US: uskhoo@hku.hken_HK
dc.identifier.authorityChan, VSF=rp01459en_HK
dc.identifier.authorityChan, KYK=rp00453en_HK
dc.identifier.authorityPoon, LLM=rp00484en_HK
dc.identifier.authorityCheung, ANY=rp00542en_HK
dc.identifier.authorityZheng, B=rp00353en_HK
dc.identifier.authorityNgan, HYS=rp00346en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.identifier.authorityChan, LC=rp00373en_HK
dc.identifier.authorityPeiris, M=rp00410en_HK
dc.identifier.authorityKhoo, US=rp00362en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/ng1698en_HK
dc.identifier.pmid16369534en_HK
dc.identifier.scopuseid_2-s2.0-29444444113en_HK
dc.identifier.hkuros112904-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29444444113&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume38en_HK
dc.identifier.issue1en_HK
dc.identifier.spage38en_HK
dc.identifier.epage46en_HK
dc.identifier.eissn1546-1718-
dc.identifier.isiWOS:000234227200015-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChan, VSF=35200370000en_HK
dc.identifier.scopusauthoridChan, KYK=7406034195en_HK
dc.identifier.scopusauthoridChen, Y=16416830300en_HK
dc.identifier.scopusauthoridPoon, LLM=7005441747en_HK
dc.identifier.scopusauthoridCheung, ANY=54927484100en_HK
dc.identifier.scopusauthoridZheng, B=7201780588en_HK
dc.identifier.scopusauthoridChan, KH=7406034307en_HK
dc.identifier.scopusauthoridMak, W=7005317285en_HK
dc.identifier.scopusauthoridNgan, HYS=34571944100en_HK
dc.identifier.scopusauthoridXu, X=9276575900en_HK
dc.identifier.scopusauthoridScreaton, G=7003284408en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK
dc.identifier.scopusauthoridAustyn, JM=7003382238en_HK
dc.identifier.scopusauthoridChan, LC=7403540707en_HK
dc.identifier.scopusauthoridYip, SP=7102133673en_HK
dc.identifier.scopusauthoridPeiris, M=7005486823en_HK
dc.identifier.scopusauthoridKhoo, US=7004195799en_HK
dc.identifier.scopusauthoridLin, CLS=37099293900en_HK
dc.identifier.citeulike451561-

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