Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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 publication




Journal article


Nat Genet

Publication Date





38 - 46


Animals, CHO Cells, Cell Adhesion Molecules, Cercopithecus aethiops, Cohort Studies, Cricetinae, Cricetulus, Genetic Predisposition to Disease, Homozygote, Hong Kong, Humans, Intestine, Small, Lectins, C-Type, Lung, Molecular Sequence Data, Proteasome Endopeptidase Complex, Receptors, Cell Surface, SARS Virus, Severe Acute Respiratory Syndrome, Tandem Repeat Sequences, Vero Cells