Virology. 2018 Jul 19;522:168-176. doi: 10.1016/j.virol.2018.07.006. [Epub ahead of print]
The p.Ser267Phe variant of sodium taurocholate cotransporting polypeptide (NTCP) supports HBV infection with a low efficiency.
Liu C1, Xu G2, Gao Z2, Zhou Z1, Guo G1, Li D2, Jing Z2, Sui J2, Li W3.
Author information
1
College of Life Sciences, Beijing Normal University, No. 19, XinJieKouWai St., HaiDian District, Beijing 100875, China; National Institute of Biological Sciences, Beijing, 7 Science Park Road ZGC Life Science Park, Beijing 102206, China.
2
National Institute of Biological Sciences, Beijing, 7 Science Park Road ZGC Life Science Park, Beijing 102206, China.
3
National Institute of Biological Sciences, Beijing, 7 Science Park Road ZGC Life Science Park, Beijing 102206, China. Electronic address: [email protected].
Abstract
Sodium taurocholate cotransporting polypeptide (NTCP) is a functional receptor for human hepatitis B virus (HBV) and its satellite virus Hepatitis D virus (HDV). Physiologically, NTCP is responsible for the majority of sodium-dependent bile acids uptake by hepatocytes. The p.Ser267Phe (S267F) variant of NTCP is a single nucleotide polymorphism (SNP) previously found to cause substantial loss of ability to support HBV and HDV infection and its taurocholic acid uptake function in vitro. Intriguingly, ten individuals were identified as S267F homozygotes in population studies of chronic hepatitis B (CHB) patients. In this study, we identified new HBV isolates from one homozygous S267F mutation carrier and confirmed new isolates also use wildtype-NTCP as a cellular receptor. Furthermore, we demonstrated S267F variant of NTCP, though inefficient, is still a functional receptor for HBV entry. This study advances our understanding of NTCP-mediated HBV infection.
KEYWORDS:
Hepatitis B virus; NTCP; Single nucleotide polymorphism; Sodium taurocholate cotransporting polypeptide; Viral receptor