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Published on: September 25, 2019
Hepatitis B virus MHBs antigen is selectively sensitive to glucosidase-mediated processing in the endoplasmic
X Lu1, Y Lu, R Geschwindt
1Department of Biochemistry and Molecular Pharmacology, The Jefferson Center of Thomas Jefferson University, Doylestown, Pennsylvania, USA.
Abstract:
Previous studies have shown that hepatitis B virus (HBV) secretion from HepG 2.2.15 cells is prevented by inhibitors of the endoplasmic reticulum (ER) glucosidase under conditions where secretion of cellular glycoproteins are not detectably affected. The 2.2.15 cells are derived from HepG2 and contain intact dimers of the viral genome. They produce and secrete infectious HBV. The secretion of the viral envelope polypeptide, MHBs, was selectively and quantitatively reduced from 2.2.15 cells in which glucosidase was inhibited, whereas the envelope polypeptide, SHBs, was relatively insensitive, being as resistant as were most host glycoproteins. Because 2.2.15 cells express all HBV ORFs, it seemed possible that the sensitivity of MHBs secretion involved its interaction with the viral nucleocapsid or other viral gene products. The work reported here showed that MHBs secretion from HepG2 cells transfected with a plasmid that expresses only the MHBs polypeptide was as sensitive to glucosidase inhibitors as it was from 2.2.15 cells. These data show that the sensitivity of the MHBs polypeptide secretion to glucosidase inhibitors is entirely encrypted within its structural gene. The reasons the MHBs polypeptide, but not SHBs, is so sensitive to glucosidase processing are discussed.
Insights
Hepatitis B virus (HBV) large envelope protein (MHBs) secretion is sensitive to ER glucosidase inhibitors. This sensitivity is inherent to the MHBs structural gene, not viral interactions.
Area of Science:
- Virology
- Cell Biology
- Biochemistry
Background:
- Hepatitis B virus (HBV) secretion is crucial for viral spread.
- Endoplasmic reticulum (ER) glucosidase inhibitors affect HBV secretion.
- Previous studies suggested viral interactions influence MHBs secretion sensitivity.
Purpose of the Study:
- To investigate the intrinsic determinants of MHBs secretion sensitivity to ER glucosidase inhibitors.
- To determine if viral gene products are necessary for MHBs secretion sensitivity.
Main Methods:
- Utilized HepG2.2.15 cells, which produce infectious HBV.
- Administered ER glucosidase inhibitors to inhibit viral protein secretion.
- Transfected HepG2 cells with a plasmid expressing only the MHBs polypeptide.
Main Results:
- ER glucosidase inhibitors selectively reduced MHBs secretion in HepG2.2.15 cells.
- SHBs secretion was relatively insensitive to glucosidase inhibition.
- MHBs secretion from HepG2 cells expressing only MHBs was equally sensitive to inhibitors.
Conclusions:
- The sensitivity of MHBs secretion to ER glucosidase inhibitors is encoded within the MHBs structural gene.
- Viral interactions are not required for this sensitivity.
- The unique sensitivity of MHBs to glucosidase processing warrants further investigation.
