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<p>The innate immune response has been reported to be perturbed by hepatitis B virus (HBV) infection. We hypothesized that the induction of the IFN-inducible dynamin family member, myxovirus resistance protein 2 (MxB), might support an innate immune response against HBV via mitochondrial alterations. The objective of this study was to elucidate the mechanism by which MxB suppresses HBV replication. Knockdown of MxB in HBV-expressing HepAD38 cells induced morphological changes in mitochondria. These cells exhibited a substantial increase in the release of enveloped HBV particles, as determined by immunoprecipitation or sucrose density-gradient centrifugation. The expression of envelope proteins L/M/SHBs was increased in the cells, and HBsAg in the culture supernatant was also increased by 4–10 fold. When cells were stimulated with poly(I: C), the downstream signaling of RIG-I including the mRNA of type I and III IFNs was suppressed. Mitochondrial antiviral signaling (MAVS) clustering, which is required for this pathway, was inhibited by MxB knockdown. In conclusion, these findings provide support for a new model implicating MxB-directed HBV inhibition initiated by downstream RIG-I signaling that could promote the formation of MAVS clusters in the mitochondria. Enhancement of this pathway could be a potential therapeutic option for suppressing HBV infection.</p>

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The interferon-inducible MxB large GTPase attenuates hepatitis B virus replication by activating the RIG-I innate immunity signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月17日

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  • Masazumi Onuki,
  • Jun Inoue,
  • Kotaro Doi,
  • Masashi Ninomiya,
  • Akitoshi Sano,
  • Mio Tsuruoka,
  • Kosuke Sato,
  • Satoko Sawahashi,
  • Keishi Ouchi,
  • Kengo Watanabe,
  • Mark A. McNiven,
  • Atsushi Masamune

摘要

The innate immune response has been reported to be perturbed by hepatitis B virus (HBV) infection. We hypothesized that the induction of the IFN-inducible dynamin family member, myxovirus resistance protein 2 (MxB), might support an innate immune response against HBV via mitochondrial alterations. The objective of this study was to elucidate the mechanism by which MxB suppresses HBV replication. Knockdown of MxB in HBV-expressing HepAD38 cells induced morphological changes in mitochondria. These cells exhibited a substantial increase in the release of enveloped HBV particles, as determined by immunoprecipitation or sucrose density-gradient centrifugation. The expression of envelope proteins L/M/SHBs was increased in the cells, and HBsAg in the culture supernatant was also increased by 4–10 fold. When cells were stimulated with poly(I: C), the downstream signaling of RIG-I including the mRNA of type I and III IFNs was suppressed. Mitochondrial antiviral signaling (MAVS) clustering, which is required for this pathway, was inhibited by MxB knockdown. In conclusion, these findings provide support for a new model implicating MxB-directed HBV inhibition initiated by downstream RIG-I signaling that could promote the formation of MAVS clusters in the mitochondria. Enhancement of this pathway could be a potential therapeutic option for suppressing HBV infection.