Related Experiment Video
Updated: Jan 8, 2026

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
The interferon-inducible MxB large GTPase attenuates hepatitis B virus replication by activating the RIG-I innate
Masazumi Onuki1, Jun Inoue2,3, Kotaro Doi1
1Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, 980-8574, Japan.
None:
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.
Related Concept Videos
Viruses with RNA Genomes
Regulation of the Unfolded Protein Response
The JAK-STAT Signaling Pathway
Experimental RNAi
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
Receptor Downregulation in MVBs
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...

