HBV受体NTCP中功能丧失的S267F变异体降低了人体对HBV感染和疾

StephenW

J Infect Dis. 2018 Jun 14. doi: 10.1093/infdis/jiy355. [Epub ahead of print]
The loss-of-function S267F variant in HBV receptor NTCP reduces human risk to HBV infection and disease progression.
An P1, Zeng Z2, Winkler CA1.
Author information

1
    Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research sponsored by the National Cancer Institute, Frederick, MD.
2
    Department of Infectious Diseases, Peking University First Hospital, Beijing, P.R. China.

Abstract
Background:

Sodium taurocholate cotransporting polypeptide (NTCP, SLC10A1) was recently identified as a hepatocyte receptor for infection of Hepatitis B virus (HBV). The natural S267F variant in NTCP causes a loss of HBV receptor function of NTCP.
Objective:

We assessed the association of S267F with HBV resistance, HBV infection clearance, and HBV-related cirrhosis and HCC.
Methods:

We tested the effects of S267F in 1117 Han Chinese patients with various HBV infection outcomes using multivariate logistic regression analysis.
Results:

The frequency of S267F (T allele) was higher in HBV-resistance healthy controls (n = 179, 4.0%) compared to HBV-infected patients (n= 648, 1.5%), with odds ratio [OR] 0.32 [95% confidence interval [CI] 0.15-0.68], p = 0.003 (dominant model). The 267F variant genotypes were also associated with reduced risk for cirrhosis (n=192, 0.5%) and HCC (n=258, 1.0% compared to those with chronic HBV infection (n=202, 3.0%), with OR 0.15 [0.03-0.70] and OR 0.21 [ 0.062-0.72], respectively. There was no association of the S267F variant with spontaneous HBV clearance.
Conclusion:

Carriage of the S267F variant for the HBV cell-entry receptor NTCP was associated with increased resistance to HBV infection and decreased risk of development of cirrhosis and liver cancer among those with chronic HBV infection.

PMID:
    29905807
DOI:
    10.1093/infdis/jiy355

StephenW

J传染病2018年6月14日doi：10.1093 / infdis / jiy355。 [电子版提前打印]
HBV受体NTCP中功能丧失的S267F变异体降低了人体对HBV感染和疾病进展的风险。
P1，曾Z2，温克勒CA1。
作者信息

1
    美国国家癌症研究所癌症研究中心基础研究实验室，Leidos生物医学研究公司，弗雷德里克癌症研究国家实验室，美国国家癌症研究所主办，弗雷德里克医学博士。
2
    北京大学第一医院感染科，北京，中国。

抽象
背景：

牛磺胆酸钠共转运多肽（NTCP，SLC10A1）最近被鉴定为乙型肝炎病毒（HBV）感染的肝细胞受体。 NTCP中的天然S267F变体导致NTCP的HBV受体功能丧失。
目的：

我们评估了S267F与HBV抗性，HBV感染清除率以及HBV相关性肝硬化和HCC的关联性。
方法：

我们使用多因素logistic回归分析检测了1117名具有各种HBV感染结果的汉族患者中S267F的作用。
结果：

与HBV感染患者（n = 648,1.5％）相比，HBV耐药健康对照（n = 179,4.0％）中S267F（T等位基因）的频率更高，优势比[OR]为0.32 [95％区间[CI] 0.15-0.68]，p = 0.003（显性模型）。与慢性HBV感染者（n = 202,3.0％）相比，267F变异基因型还与肝硬化风险降低（n = 192，0.5％）和HCC相关（n = 258,1.0％），OR 0.15 [0.03 -0.70]和OR 0.21 [0.062-0.72]，S267F变异与自发性HBV清除无关。
结论：

携带乙型肝炎病毒进入受体NTCP的S267F变体与慢性乙型肝炎病毒感染者的HBV感染抵抗力增加和肝硬化和肝癌发生风险降低相关。

结论：
    29905807
DOI：
    10.1093 / infdis / jiy355