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ATP1B3 Restricts Hepatitis B Virus Replication Via Reducing the Expression of the Envelope Proteins

Jun Zhang1, Tianhang Zheng1, Xiaolei Zhou1

  • 1Institute of Virology and AIDS Research, the First Hospital of Jilin University, Changchun, 130021, China.

Virologica Sinica
|February 3, 2021
PubMed

Insights

ATP1B3 protein degrades hepatitis B virus (HBV) envelope proteins via the proteasome pathway, offering a new therapeutic target for HBV infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • ATP1B3 was previously shown to inhibit hepatitis B virus (HBV) replication through NF-κB activation.
  • Mutant ATP1B3 proteins, despite lacking NF-κB activation, still suppressed HBV replication, indicating an alternative mechanism.
  • This study investigates the uncharacterized pathway of ATP1B3-mediated HBV suppression.

Purpose of the Study:

  • To elucidate the novel mechanism by which ATP1B3 suppresses HBV replication.
  • To investigate the role of ATP1B3 in the degradation of HBV envelope proteins.
  • To explore the potential of ATP1B3 as a therapeutic target for HBV infection.

Main Methods:

  • Western blotting to assess HBV envelope protein expression.
  • Proteasome inhibitor MG132 treatment to evaluate protein degradation pathways.
  • Co-immunoprecipitation (Co-IP) assays to detect protein interactions and ubiquitination.
  • Immunofluorescence microscopy for co-localization studies.

Main Results:

  • ATP1B3 significantly reduced the expression of HBV envelope proteins (LHBs, MHBs, SHBs).
  • Proteasome inhibition by MG132 rescued the degradation of envelope proteins, implicating the proteasome pathway.
  • ATP1B3 was found to interact with and induce polyubiquitination of LHBs and MHBs.
  • Co-localization of ATP1B3 with LHBs and MHBs was confirmed.

Conclusions:

  • ATP1B3 suppresses HBV replication by promoting the proteasome-dependent degradation of HBV envelope proteins.
  • ATP1B3 interacts with and polyubiquitinates HBV envelope proteins, marking them for degradation.
  • Targeting ATP1B3 presents a promising therapeutic strategy for managing HBV infection.
Keywords:
ATP1B3Envelope proteinsHepatitis B virus (HBV)Proteasome-dependent degradation

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