Toll样受体3（TLR3）基因的多态性与高加索人群中乙型肝炎病

StephenW

Sci Rep. 2018 Aug 24;8(1):12737. doi: 10.1038/s41598-018-31065-6.
Polymorphisms in the Toll-like receptor 3 (TLR3) gene are associated with the natural course of hepatitis B virus infection in Caucasian population.
Fischer J1, Koukoulioti E2, Schott E3, Fülöp B4, Heyne R5, Berg T2, van Bömmel F2.
Author information

1
    Department of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany. [email protected].
2
    Department of Gastroenterology and Rheumatology, Section of Hepatology, University Hospital Leipzig, Leipzig, Germany.
3
    Department of Gastroenterology, Hepatology and Diabetology, Internal Medicine II, HELIOS Hospital Emil von Behring, Berlin, Germany.
4
    Department of Internal Medicine and Gastroenterology, HELIOS Hospital Berlin-Buch, Berlin, Germany.
5
    Liver and Study Center Checkpoint, Berlin, Germany.

Abstract

Innate immunity can induce spontaneous hepatitis B surface antigen (HBsAg) seroclearance (SC) of hepatitis B virus (HBV) infection or transition towards an inactive carrier state. Toll-like receptor (TLR) 3 signalling has been linked to these processes. Alterations in the TLR3 gene might impair immune responses against HBV. In our study, we analysed the impact of the TLR3 polymorphisms rs3775291 and rs5743305 on the natural course of HBV infection. In this retrospective study, a Caucasian cohort of 621 patients with chronic HBV infection (CHB), 239 individuals with spontaneous HBsAg SC, and 254 healthy controls were enrolled. In the CHB group, 49% of patients were inactive carriers, and 17% were HBeAg-positive. The TLR3 rs3775291 A allele was associated with a reduced likelihood of spontaneous HBsAg SC and HBeAg SC, and an increased risk of developing chronic hepatitis B. In haplotype analysis, the haplotype including both risk variants rs3775291A and rs5743305A had the lowest likelihood of HBsAg SC. Further research in larger cohorts and functional analyses are needed to shed light on the impact of TLR3 signalling.

PMID:
    30143709
DOI:
    10.1038/s41598-018-31065-6

StephenW

Sci Rep.2018 8月24日; 8（1）：12737。 doi：10.1038 / s41598-018-31065-6。
Toll样受体3（TLR3）基因的多态性与高加索人群中乙型肝炎病毒感染的自然过程有关。
Fischer J1，Koukoulioti E2，Schott E3，FülöpB4，Heyne R5，Berg T2，vanBömmelF2。
作者信息

1
    德国莱比锡莱比锡大学医院肝病科消化内科和风湿病科。 [email protected]。
2
    德国莱比锡莱比锡大学医院肝病科消化内科和风湿病科。
3
    消化内科，肝脏病学和糖尿病学，内科学II，HELIOS医院Emil von Behring，德国柏林。
4
    德国柏林柏林赫希医院内科和胃肠病学系。
五
    肝脏和研究中心检查站，柏林，德国。

抽象

先天免疫可诱导乙型肝炎病毒（HBV）感染的自发性乙型肝炎表面抗原（HBsAg）血清清除（SC）或向无活性载体状态转变。 Toll样受体（TLR）3信号传导与这些过程有关。 TLR3基因的改变可能会削弱针对HBV的免疫应答。在我们的研究中，我们分析了TLR3多态性rs3775291和rs5743305对HBV感染的自然过程的影响。在这项回顾性研究中，招募了621名患有慢性HBV感染（CHB）的患者，239名患有自发性HBsAg SC的个体和254名健康对照的高加索人群。在CHB组中，49％的患者为非活动性携带者，17％的患者为HBeAg阳性。 TLR3 rs3775291 A等位基因与自发性HBsAg SC和HBeAg SC的可能性降低相关，并且发生慢性乙型肝炎的风险增加。在单倍型分析中，包括风险变体rs3775291A和rs5743305A的单倍型具有最低的HBsAg SC可能性。需要进一步研究更大的队列和功能分析，以阐明TLR3信号传导的影响。

结论：
    30143709
DOI：
    10.1038 / s41598-018-31065-6

StephenW

https://www.nature.com/articles/s41598-018-31065-6