Homozygous L-SIGN (CLEC4M) plays a protective role in SARS coronavirus infection |
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Authors: | Chan Vera S F Chan Kelvin Y K Chen Yongxiong Poon Leo L M Cheung Annie N Y Zheng Bojian Chan Kwok-Hung Mak William Ngan Hextan Y S Xu Xiaoning Screaton Gavin Tam Paul K H Austyn Jonathan M Chan Li-Chong Yip Shea-Ping Peiris Malik Khoo Ui-Soon Lin Chen-Lung S |
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Affiliation: | Department of Surgery, Hong Kong Jockey Club Clinical Research Center, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong, SAR, China. |
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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. |
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