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<p>RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication.</p>

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A double-edged sword in antiviral defence: ATG7 binding dicer to promote virus replication

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年2月22日

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  • Yaotang Wu,
  • Yang Wu,
  • Chenlu Wang,
  • Ningna Xiong,
  • Wenxin Ji,
  • Mei Fu,
  • Junpeng Zhu,
  • Zhixin Li,
  • Jian Lin,
  • Qian Yang

摘要

RNA interference (RNAi) and autophagy are two pivotal biological processes that regulate virus replication. This study explored the complex relationship between autophagy and RNAi in controlling influenza virus replication. Initially, we reported that influenza virus (H9N2) infection increases the viral load and the expression of autophagy markers while inhibiting the RNAi pathway. Subsequent studies employing autophagy enhancer and inhibitor treatments confirmed that avian influenza virus (AIV, H9N2) promotes viral replication by enhancing autophagy pathways. Further analysis revealed that ATG7, an autophagy protein, can interact with dicer to affect its antiviral functions. Finally, we discovered that infection with other avian RNA viruses, including infectious bursal disease virus (IBDV) and infectious bronchitis virus (IBV), induced the upregulation of ATG7, which blocked the RNAi pathway to facilitate virus replication. Our findings suggested that virus infection might trigger the upregulation of autophagy and downregulation of the RNAi pathway, revealing a complex interaction between these two biological processes in the defence against viral replication.