Effect of S267F variant of NTCP on the patients with chronic hepatitis B

Hye Won Lee, Hye Jung Park, Bora Jin, Mehrangiz Dezhbord, Do Young Kim, Kwang Hyub Han, Wang Shick Ryu, Seungtaek Kim, Sang Hoon Ahn

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16 Citations (Scopus)


Sodium taurocholate cotransporting polypeptide (NTCP) was identified as an entry receptor for hepatitis B virus (HBV) infection. The substitution of serine at position 267 of NTCP with phenylalanine (S267F) is an Asian-specific variation that hampers HBV entry in vitro. In this study, we aimed to evaluate the prevalence of S267F polymorphism in Korean patients with chronic hepatitis B (CHB) and its association with disease progression and potential viral evolution in the preS1 domain of HBV. We found that the frequency of the S267F variant of NTCP in CHB patients and controls was 2.7% and 5.7% (P = 0.031), respectively, and that those who had S267F variant were less susceptible to chronic HBV infection. The frequency of the S267F variant in CHB, cirrhosis and hepatocellular carcinoma (HCC) patients was 3.3%, 0.9%, and 3.5%, respectively. Thus, the S267F variant correlated significantly with a lower risk for cirrhosis (P = 0.036). Sequencing preS1 domain of HBV from the patients who had S267F variant revealed no significant sequence change compared to the wild type. In conclusion, the S267F variant of NTCP is clinically associated with a lower risk of chronic HBV infection and cirrhosis development, which implicates suppressing HBV entry could reduce the disease burden.

Original languageEnglish
Article number17634
JournalScientific reports
Issue number1
Publication statusPublished - 2017 Dec 1

Bibliographical note

Funding Information:
We are grateful to Dr. Kyun-Hwan Kim and Dr. Chul Hoon Kim for their critical review of this manuscript. This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (No. 2013R1A1A2008346, No. 2016R1A2B1009847) (S.K.) and Daewoong Pharmaceutical (2015-31-0695), Yuhan (2015-31-0061), Handok (2015-31-0870) (S.H.A.).

Publisher Copyright:
© 2017 The Author(s).

All Science Journal Classification (ASJC) codes

  • General


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