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

Vera S.F. Chan, Kelvin Y.K. Chan, Yongxiong Chen, Leo L.M. Poon, Annie N.Y. Cheung, Bojian Zheng, Kwok Hung Chan, William Mak, Hextan Y.S. Ngan, Xiaoning Xu, Gavin Screaton, Paul K.H. Tam, Jonathan M. Austyn, Li Chong Chan, Shea Ping Yip, Malik Peiris, Ui Soon Khoo, Chen Lung S. Lin

Research output: Journal article publicationJournal articleAcademic researchpeer-review

110 Citations (Scopus)

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.
Original languageEnglish
Pages (from-to)38-46
Number of pages9
JournalNature Genetics
Volume38
Issue number1
DOIs
Publication statusPublished - 1 Jan 2006

ASJC Scopus subject areas

  • Genetics

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