Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/26557
Title: Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection
Authors: Chan, VSF
Chan, KYK
Chen, Y
Poon, LLM
Cheung, ANY
Zheng, B
Chan, KH
Mak, W
Ngan, HYS
Xu, X
Screaton, G
Tam, PKH
Austyn, JM
Chan, LC
Yip, SP 
Peiris, M
Khoo, US
Lin, CLS
Issue Date: 2006
Source: Nature genetics, 2006, v. 38, no. 1, p. 38-46 How to cite?
Journal: Nature genetics 
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.
URI: http://hdl.handle.net/10397/26557
ISSN: 1061-4036
DOI: 10.1038/ng1698
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