乙型肝炎病毒大表面蛋白：功能与名气。
Hepatitis B virus large surface protein: function and fame.
机构信息
Department of Gastroenterology, Justus Liebig University, Giessen, Germany.
出版信息
Hepatobiliary Surg Nutr. 2015 Feb;4(1):1-10. doi: 10.3978/j.issn.2304-3881.2014.12.08.
Abstract
Chronic infection with hepatitis B virus (HBV) is the leading cause of liver cirrhosis and hepatocellular carcinoma worldwide. HBV life cycle begins with viral attachment to hepatocytes, mediated by the large HBV surface protein (LHBs). Identification of the sodium-taurocholate cotransporting polypeptide (NTCP) as a HBV receptor has revealed a suitable target for viral entry inhibition. Analysis of serum hepatitis B surface antigen (HBsAg) level is a non-invasive diagnostic parameter that improves HBV treatment opportunities. Furthermore, HBsAg plays an important role in manipulation of host immune response by HBV. However, observations in patients with chronic hepatitis B under conditions of immune suppression and in transgenic mouse models of HBV infection suggest, that in absence of adaptive immune responses cellular mechanisms induced by HBV may also lead to the development of liver diseases. Thus, the multifaceted pathological aspects of HBsAg predetermine the design of new therapeutical options modulating associated biological implications.
摘要
慢性乙型肝炎病毒（HBV）感染是全球肝硬化和肝细胞癌的主要原因。HBV 生命周期始于病毒与肝细胞的附着，这一过程由大 HBV 表面蛋白（LHBs）介导。钠离子牛磺胆酸共转运多肽（NTCP）作为 HBV 受体的鉴定揭示了病毒进入抑制的合适靶点。血清乙型肝炎表面抗原（HBsAg）水平分析是一种非侵入性诊断参数，可改善 HBV 治疗机会。此外，HBsAg 在 HBV 对宿主免疫反应的调控中发挥着重要作用。然而，在免疫抑制患者和 HBV 感染的转基因小鼠模型中的观察结果表明，在缺乏适应性免疫反应的情况下，HBV 诱导的细胞机制也可能导致肝病的发生。因此，HBsAg 的多方面病理特征决定了设计新的治疗方案来调节相关的生物学意义。
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Monocytes from chronic HBV patients react in vitro to HBsAg and TLR by producing cytokines irrespective of stage of disease.慢性乙肝患者的单核细胞在体外对乙肝表面抗原（HBsAg）和Toll样受体（TLR）产生反应，分泌细胞因子，且不受疾病阶段影响。
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