Abstract <p>hnRNPA2/B1 is an RNA-binding protein involved in the regulation of transcription, mRNA stability, and also functions as one of the regulators of the intracellular antiviral response. Its role in intranuclear recognition of foreign DNA from herpes simplex virus type 1 as well as in the initiation and amplification of antiviral signaling cascades has been demonstrated. In this study, we have shown for the first time the relocalization of hnRNPA2B1 mRNA from the nucleus to the cytoplasm in cells supporting hepatitis B virus (HBV) replication. We have also demonstrated, for the first time, the anti-HBV activity of hnRNPA2B1 and its ability to destabilize the major HBV transcript. Notably, in HBV model systems, hnRNPA2B1 did not alter the expression or localization of mRNAs encoding antiviral factors. The suppression of HBV replication was not accompanied by changes in interferon-β production. Taken together, hnRNPA2B1 exerts an antiviral activity in HBV models, and its mechanism of action is not associated with the activation of intracellular antiviral cascades or pathways analogous to intranuclear recognition of the herpes simplex virus DNA.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

The Role of hnRNPA2/B1 in Hepatitis B Virus Replication and Transcription

  • I. V. Karandashov,
  • S. A. Brezgin,
  • N. I. Ponomareva,
  • A. S. Frolova,
  • V. P. Chulanov,
  • A. P. Kostyusheva,
  • D. S. Kostyushev

摘要

Abstract

hnRNPA2/B1 is an RNA-binding protein involved in the regulation of transcription, mRNA stability, and also functions as one of the regulators of the intracellular antiviral response. Its role in intranuclear recognition of foreign DNA from herpes simplex virus type 1 as well as in the initiation and amplification of antiviral signaling cascades has been demonstrated. In this study, we have shown for the first time the relocalization of hnRNPA2B1 mRNA from the nucleus to the cytoplasm in cells supporting hepatitis B virus (HBV) replication. We have also demonstrated, for the first time, the anti-HBV activity of hnRNPA2B1 and its ability to destabilize the major HBV transcript. Notably, in HBV model systems, hnRNPA2B1 did not alter the expression or localization of mRNAs encoding antiviral factors. The suppression of HBV replication was not accompanied by changes in interferon-β production. Taken together, hnRNPA2B1 exerts an antiviral activity in HBV models, and its mechanism of action is not associated with the activation of intracellular antiviral cascades or pathways analogous to intranuclear recognition of the herpes simplex virus DNA.