title: Mannose-binding lectin in severe acute respiratory syndrome coronavirus infection.
abstract: Little is known about the innate immune response to severe acute respiratory syndrome (SARS) coronavirus (CoV) infection. Mannose-binding lectin (MBL), a key molecule in innate immunity, functions as an ante-antibody before the specific antibody response. Here, we describe a case-control study that included 569 patients with SARS and 1188 control subjects and used in vitro assays to investigate the role that MBL plays in SARS-CoV infection. The distribution of MBL gene polymorphisms was significantly different between patients with SARS and control subjects, with a higher frequency of haplotypes associated with low or deficient serum levels of MBL in patients with SARS than in control subjects. Serum levels of MBL were also significantly lower in patients with SARS than in control subjects. There was, however, no association between MBL genotypes, which are associated with low or deficient serum levels of MBL, and mortality related to SARS. MBL could bind SARS-CoV in a dose- and calcium-dependent and mannan-inhibitable fashion in vitro, suggesting that binding is through the carbohydrate recognition domains of MBL. Furthermore, deposition of complement C4 on SARS-CoV was enhanced by MBL. Inhibition of the infectivity of SARS-CoV by MBL in fetal rhesus kidney cells (FRhK-4) was also observed. These results suggest that MBL contributes to the first-line host defense against SARS-CoV and that MBL deficiency is a susceptibility factor for acquisition of SARS.
authors.affiliation: Department of Paediatrics and Adolescent Medicine, The University of Hong Kong, China.
authors.forename: W K Eddie
authors.initials: WK
authors.lastname: Ip
authors.forename: Kwok Hung
authors.initials: KH
authors.lastname: Chan
authors.forename: Helen K W
authors.initials: HK
authors.lastname: Law
authors.forename: Gloria H W
authors.initials: GH
authors.lastname: Tso
authors.forename: Eric K P
authors.initials: EK
authors.lastname: Kong
authors.forename: Wilfred H S
authors.initials: WH
authors.lastname: Wong
authors.forename: Yuk Fai
authors.initials: YF
authors.lastname: To
authors.forename: Raymond W H
authors.initials: RW
authors.lastname: Yung
authors.forename: Eudora Y
authors.initials: EY
authors.lastname: Chow
authors.forename: Ka Leung
authors.initials: KL
authors.lastname: Au
authors.forename: Eric Y T
authors.initials: EY
authors.lastname: Chan
authors.forename: Wilina
authors.initials: W
authors.lastname: Lim
authors.forename: Jens C
authors.initials: JC
authors.lastname: Jensenius
authors.forename: Malcolm W
authors.initials: MW
authors.lastname: Turner
authors.forename: J S Malik
authors.initials: JS
authors.lastname: Peiris
authors.forename: Yu Lung
authors.initials: YL
authors.lastname: Lau
mesh_terms: D000328:Adult; D003167:Complement Activation; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D037601:Mannose-Binding Lectin / Q000097:blood* / Q000235:genetics*; D011485:Protein Binding; D045169:Severe Acute Respiratory Syndrome / Q000235:genetics* / Q000276:immunology*
chemical_list: D037601:Mannose-Binding Lectin