C-type lectin LSECtin interacts with DC-SIGNR and is involved in hepatitis C virus binding.
Hepatitis C virus (HCV) is a major cause of liver disease. However, the detailed mechanism underlying hepatocyte infection with HCV is not yet completely understood. We previously identified a novel C-type lectin--LSECtin predominantly expressed on liver sinusoidal endothelial cells. Here we demonstrate that LSECtin can interact with two HCV receptors, DC-SIGNR and CD81, through its central ectodomain. Furthermore, cells expressing LSECtin specifically can be attached by the naturally occurring HCV in the sera of infected individuals. This binding was found to be mediated by the HCV E2 glycoprotein and could be efficiently inhibited by EGTA but not by mannan treatment. The present study suggests that LSECtin interaction with DC-SIGNR might contribute to HCV binding to liver sinusoidal endothelial cells.
Li
Yi
Y
State Key Laboratory of Proteomics, Beijing Proteome Research Center, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Hao
Bingtao
B
Kuai
Xuezhang
X
Xing
Guichun
G
Yang
Juntao
J
Chen
Jie
J
Tang
Li
L
Zhang
Lingqiang
L
He
Fuchu
F
D000818:Animals; D001665:Binding Sites; D016466:CHO Cells; D006224:Cricetinae; D003412:Cricetulus; D042783:Endothelial Cells / Q000378:metabolism; D016174:Hepacivirus / Q000378:metabolism* / Q000472:pathogenicity; D006801:Humans; D037181:Lectins, C-Type / Q000378:metabolism*; D051379:Mice; D041681:NIH 3T3 Cells; D011956:Receptors, Cell Surface / Q000378:metabolism*; D014759:Viral Envelope Proteins / Q000378:metabolism
D037181:Lectins, C-Type; D011956:Receptors, Cell Surface; D014759:Viral Envelope Proteins; C091015:glycoprotein E2, Hepatitis C virus