乙肝表面抗原块I型干扰素诱导上调通过抑制STAT3的A3G的

StephenW

Biochem Biophys Res Commun. 2016 Mar 18. pii: S0006-291X(16)30393-X. doi: 10.1016/j.bbrc.2016.03.082. [Epub ahead of print]
HBsAg blocks TYPE I IFN induced up-regulation of A3G through inhibition of STAT3.Xu F1, Song H1, Li N2, Tan G3.
Author information

• 1Institute of Translational Medicine, Department of Immunology, The First Hospital, Jilin University, Changchun, Jilin, 130061, PR China.
• 2Department of Obstetric, The First Hospital, Jilin University, Changchun, Jilin, 130021, PR China.
• 3Institute of Translational Medicine, Department of Immunology, The First Hospital, Jilin University, Changchun, Jilin, 130061, PR China. Electronic address: [email protected].
  

AbstractInterferon (IFN) is a regularly utilized therapeutic for the treatment of chronic hepatitis B and appears to induce superior HBeAg seroconversion comparing nucleos/tide analogues. However, the mechanisms underlying IFN inhibition of HBV replication, as well as poor responses to IFN are unclear. Apobec3G has been reported to be involved in regulating HBV replication. In this study, we investigated Apobec3G expression and regulatory pathways during HBV infection. We show that over-expression of A3G leads to inhibition of HBV replication. We also show that IFN induces a significant increase in A3G protein expression, which is associated with STAT3 activation. We further show that A3G expression in HBV patients is lower compared to non-infected controls, possibly by HBsAg which inhibits IFN induced A3G up-regulation in a dose dependent manner. This process is likely mediated through inhibition of STAT3-Ser727 phosphorylation. The results presented in this study indicate that STAT3 plays an important role in IFN-induced A3G production, and HBsAg may correlated with poor response to IFN treatment.
Copyright © 2016. Published by Elsevier Inc.


KEYWORDS: A3G; HBV; HBs; STAT3

StephenW

生物化学与生物物理学研究通讯。 2016年18月PII：S0006-291X（16）30393-X。 DOI：10.1016 / j.bbrc.2016.03.082。 [打印EPUB提前]
乙肝表面抗原块I型干扰素诱导上调通过抑制STAT3的A3G的。
许F1，宋H1，李N2，谭G3。
作者信息

    转化医学，免疫学系，第一医院，吉林大学，长春，吉林，130061，PR中国的1Institute。
    产科第一医院，吉林大学，长春，吉林，130021，PR中国教研室。
    转化医学，免疫学系，第一医院，吉林大学，长春，吉林，130061，PR中国的3Institute。电子地址：[email protected]。

抽象

干扰素（IFN）是一种利用定期治疗慢性乙型肝炎的治疗，并出现诱导优越的HBeAg血清转换比较核苷/潮类似物。然而，底层HBV复制的干扰素抑制机制，以及差响应干扰素目前还不清楚。 APOBEC3G已报道参与调节HBV复制。在这项研究中，我们HBV感染调查期间表达APOBEC3G和监管途径。我们证明了过表达A3G的导致抑制HBV的复制。我们还表明，干扰素诱导A3G蛋白表达，这是与STAT3的活化相关联的显著增加。进一步的研究表明在乙型肝炎患者A3G表达相比降低至未感染的控制，有可能通过的HBsAg抑制干扰素诱导A3G上调以剂量依赖性的方式。这个过程是通过抑制STAT3-Ser727磷酸化可能介导的。在本研究中提出的结果表明STAT3起着IFN-诱导A3G生产中起重要作用，与HBsAg可以与对IFN治疗反应差相关。

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关键词：

A3G;乙肝病毒; HBs抗体; STAT3