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- Publisher Website: 10.1038/ng1698
- Scopus: eid_2-s2.0-29444444113
- PMID: 16369534
- WOS: WOS:000234227200015
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Article: Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
Title | Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection |
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Authors | |
Keywords | Species Index: Animalia Coronavirus Sars Coronavirus |
Issue Date | 2006 |
Publisher | Nature 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 Identifier | http://hdl.handle.net/10722/132497 |
ISSN | 2023 Impact Factor: 31.7 2023 SCImago Journal Rankings: 17.300 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Chan, VSF | en_HK |
dc.contributor.author | Chan, KYK | en_HK |
dc.contributor.author | Chen, Y | en_HK |
dc.contributor.author | Poon, LLM | en_HK |
dc.contributor.author | Cheung, ANY | en_HK |
dc.contributor.author | Zheng, B | en_HK |
dc.contributor.author | Chan, KH | en_HK |
dc.contributor.author | Mak, W | en_HK |
dc.contributor.author | Ngan, HYS | en_HK |
dc.contributor.author | Xu, X | en_HK |
dc.contributor.author | Screaton, G | en_HK |
dc.contributor.author | Tam, PKH | en_HK |
dc.contributor.author | Austyn, JM | en_HK |
dc.contributor.author | Chan, LC | en_HK |
dc.contributor.author | Yip, SP | en_HK |
dc.contributor.author | Peiris, M | en_HK |
dc.contributor.author | Khoo, US | en_HK |
dc.contributor.author | Lin, CLS | en_HK |
dc.date.accessioned | 2011-03-28T09:25:26Z | - |
dc.date.available | 2011-03-28T09:25:26Z | - |
dc.date.issued | 2006 | en_HK |
dc.identifier.citation | Nature Genetics, 2006, v. 38 n. 1, p. 38-46 | en_HK |
dc.identifier.issn | 1061-4036 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/132497 | - |
dc.description.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. | en_HK |
dc.language | eng | en_US |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.genetics.nature.com | en_HK |
dc.relation.ispartof | Nature Genetics | en_HK |
dc.subject | Species Index: Animalia | en_US |
dc.subject | Coronavirus | en_US |
dc.subject | Sars Coronavirus | en_US |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | CHO Cells - virology | en_HK |
dc.subject.mesh | Cell Adhesion Molecules - genetics - metabolism | en_HK |
dc.subject.mesh | Cercopithecus aethiops | en_HK |
dc.subject.mesh | Cohort Studies | en_HK |
dc.subject.mesh | Cricetinae | en_HK |
dc.subject.mesh | Cricetulus | en_HK |
dc.subject.mesh | Genetic Predisposition to Disease | en_HK |
dc.subject.mesh | Homozygote | en_HK |
dc.subject.mesh | Hong Kong - epidemiology | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Intestine, Small - physiology | en_HK |
dc.subject.mesh | Lectins, C-Type - genetics - metabolism | en_HK |
dc.subject.mesh | Lung - physiology - virology | en_HK |
dc.subject.mesh | Molecular Sequence Data | en_HK |
dc.subject.mesh | Proteasome Endopeptidase Complex - metabolism | en_HK |
dc.subject.mesh | Receptors, Cell Surface - genetics - metabolism | en_HK |
dc.subject.mesh | SARS Virus - metabolism - pathogenicity | en_HK |
dc.subject.mesh | Severe Acute Respiratory Syndrome - epidemiology - genetics | en_HK |
dc.subject.mesh | Tandem Repeat Sequences | en_HK |
dc.subject.mesh | Vero Cells - virology | en_HK |
dc.title | Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Chan, VSF: sfvchan@hku.hk | en_HK |
dc.identifier.email | Chan, KYK: kelvinc@pathology.hku.hk | en_HK |
dc.identifier.email | Poon, LLM: llmpoon@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, ANY: anycheun@hkucc.hku.hk | en_HK |
dc.identifier.email | Zheng, B: bzheng@hkucc.hku.hk | en_HK |
dc.identifier.email | Ngan, HYS: hysngan@hkucc.hku.hk | en_HK |
dc.identifier.email | Tam, PKH: paultam@hku.hk | en_HK |
dc.identifier.email | Chan, LC: chanlc@hkucc.hku.hk | en_HK |
dc.identifier.email | Peiris, M: malik@hkucc.hku.hk | en_HK |
dc.identifier.email | Khoo, US: uskhoo@hku.hk | en_HK |
dc.identifier.authority | Chan, VSF=rp01459 | en_HK |
dc.identifier.authority | Chan, KYK=rp00453 | en_HK |
dc.identifier.authority | Poon, LLM=rp00484 | en_HK |
dc.identifier.authority | Cheung, ANY=rp00542 | en_HK |
dc.identifier.authority | Zheng, B=rp00353 | en_HK |
dc.identifier.authority | Ngan, HYS=rp00346 | en_HK |
dc.identifier.authority | Tam, PKH=rp00060 | en_HK |
dc.identifier.authority | Chan, LC=rp00373 | en_HK |
dc.identifier.authority | Peiris, M=rp00410 | en_HK |
dc.identifier.authority | Khoo, US=rp00362 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1038/ng1698 | en_HK |
dc.identifier.pmid | 16369534 | - |
dc.identifier.scopus | eid_2-s2.0-29444444113 | en_HK |
dc.identifier.hkuros | 112904 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-29444444113&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 38 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 38 | en_HK |
dc.identifier.epage | 46 | en_HK |
dc.identifier.eissn | 1546-1718 | - |
dc.identifier.isi | WOS:000234227200015 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Chan, VSF=35200370000 | en_HK |
dc.identifier.scopusauthorid | Chan, KYK=7406034195 | en_HK |
dc.identifier.scopusauthorid | Chen, Y=16416830300 | en_HK |
dc.identifier.scopusauthorid | Poon, LLM=7005441747 | en_HK |
dc.identifier.scopusauthorid | Cheung, ANY=54927484100 | en_HK |
dc.identifier.scopusauthorid | Zheng, B=7201780588 | en_HK |
dc.identifier.scopusauthorid | Chan, KH=7406034307 | en_HK |
dc.identifier.scopusauthorid | Mak, W=7005317285 | en_HK |
dc.identifier.scopusauthorid | Ngan, HYS=34571944100 | en_HK |
dc.identifier.scopusauthorid | Xu, X=9276575900 | en_HK |
dc.identifier.scopusauthorid | Screaton, G=7003284408 | en_HK |
dc.identifier.scopusauthorid | Tam, PKH=7202539421 | en_HK |
dc.identifier.scopusauthorid | Austyn, JM=7003382238 | en_HK |
dc.identifier.scopusauthorid | Chan, LC=7403540707 | en_HK |
dc.identifier.scopusauthorid | Yip, SP=7102133673 | en_HK |
dc.identifier.scopusauthorid | Peiris, M=7005486823 | en_HK |
dc.identifier.scopusauthorid | Khoo, US=7004195799 | en_HK |
dc.identifier.scopusauthorid | Lin, CLS=37099293900 | en_HK |
dc.identifier.citeulike | 451561 | - |
dc.identifier.issnl | 1061-4036 | - |