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

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TitleHomozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
AuthorsChan, VSF1
Chan, KYK1
Chen, Y1
Poon, LLM1
Cheung, ANY1
Zheng, B1
Chan, KH1
Mak, W1
Ngan, HYS1
Xu, X4
Screaton, G2
Tam, PKH1
Austyn, JM3
Chan, LC1
Yip, SP5
Peiris, M1
Khoo, US1
Lin, CLS1
KeywordsSpecies Index: Animalia
Coronavirus
Sars Coronavirus
Issue Date2006
PublisherNature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com
CitationNature Genetics, 2006, v. 38 n. 1, p. 38-46 [How to Cite?]
DOI: http://dx.doi.org/10.1038/ng1698
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.
ISSN1061-4036
2011 Impact Factor: 35.532
2011 SCImago Journal Rankings: 8.923
DOIhttp://dx.doi.org/10.1038/ng1698
ISI Accession Number IDWOS:000234227200015
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorChan, VSF
dc.contributor.authorChan, KYK
dc.contributor.authorChen, Y
dc.contributor.authorPoon, LLM
dc.contributor.authorCheung, ANY
dc.contributor.authorZheng, B
dc.contributor.authorChan, KH
dc.contributor.authorMak, W
dc.contributor.authorNgan, HYS
dc.contributor.authorXu, X
dc.contributor.authorScreaton, G
dc.contributor.authorTam, PKH
dc.contributor.authorAustyn, JM
dc.contributor.authorChan, LC
dc.contributor.authorYip, SP
dc.contributor.authorPeiris, M
dc.contributor.authorKhoo, US
dc.contributor.authorLin, CLS
dc.date.accessioned2011-03-28T09:25:26Z
dc.date.available2011-03-28T09:25:26Z
dc.date.issued2006
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.
dc.description.naturelink_to_subscribed_fulltext
dc.identifier.citationNature Genetics, 2006, v. 38 n. 1, p. 38-46 [How to Cite?]
DOI: http://dx.doi.org/10.1038/ng1698
dc.identifier.citeulike451561
dc.identifier.doihttp://dx.doi.org/10.1038/ng1698
dc.identifier.eissn1546-1718
dc.identifier.epage46
dc.identifier.hkuros112904
dc.identifier.isiWOS:000234227200015
dc.identifier.issn1061-4036
2011 Impact Factor: 35.532
2011 SCImago Journal Rankings: 8.923
dc.identifier.issue1
dc.identifier.pmid16369534
dc.identifier.scopuseid_2-s2.0-29444444113
dc.identifier.spage38
dc.identifier.urihttp://hdl.handle.net/10722/132497
dc.identifier.volume38
dc.languageeng
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com
dc.publisher.placeUnited States
dc.relation.ispartofNature Genetics
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshCHO Cells - virology
dc.subject.meshCell Adhesion Molecules - genetics - metabolism
dc.subject.meshCercopithecus aethiops
dc.subject.meshCohort Studies
dc.subject.meshCricetinae
dc.subject.meshCricetulus
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshHomozygote
dc.subject.meshHong Kong - epidemiology
dc.subject.meshHumans
dc.subject.meshIntestine, Small - physiology
dc.subject.meshLectins, C-Type - genetics - metabolism
dc.subject.meshLung - physiology - virology
dc.subject.meshMolecular Sequence Data
dc.subject.meshProteasome Endopeptidase Complex - metabolism
dc.subject.meshReceptors, Cell Surface - genetics - metabolism
dc.subject.meshSARS Virus - metabolism - pathogenicity
dc.subject.meshSevere Acute Respiratory Syndrome - epidemiology - genetics
dc.subject.meshTandem Repeat Sequences
dc.subject.meshVero Cells - virology
dc.subjectSpecies Index: Animalia
dc.subjectCoronavirus
dc.subjectSars Coronavirus
dc.titleHomozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Imperial College London
  3. Nuffield Department of Clinical Medicine
  4. Weatherall Institute of Molecular Medicine
  5. Hong Kong Polytechnic University