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Host-derived intracellular immunization against mouse hepatitis virus infection
W Chen1, V J Madden, C R Bagnell
1Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill 27599, USA.
Virology
|February 17, 1997
Summary
Mouse hepatitis virus (MHV) entry relies on the biliary glycoprotein receptor (BgpA). Overexpressing BgpA in cells traps viruses, blocking infectious progeny release by hindering spike glycoprotein maturation.
Area of Science:
- Virology
- Cell Biology
- Immunology
Background:
- Mouse hepatitis virus (MHV) uses the biliary glycoprotein receptor (BgpA) for cell entry.
- Understanding MHV-BgpA interactions is crucial for viral pathogenesis research.
Purpose of the Study:
- To investigate the role of BgpA receptor levels in MHV-A59 replication and progeny virion formation.
- To elucidate the mechanism by which BgpA affects MHV maturation and release.
Main Methods:
- Transfection of Bgp1 gene into murine DBT cells to create varying levels of BgpA receptor expression.
- Infection of engineered cell clones with MHV-A59.
- Treatment with monoclonal antibody CC1.
- Viral titration, transcription analysis, and ultrastructural studies.
- Analysis of viral protein composition (S, N, M glycoproteins).
Main Results:
- BgpA receptor overexpression in DBT cells reduced infectious MHV progeny virion release.
- Virus transcription remained unaffected, suggesting a post-transcriptional block.
- Ultrastructural analysis showed reduced peplomer spike glycoproteins on virions from overexpressing cells.
- Monoclonal antibody CC1 reversed the inhibitory effect of BgpA overexpression.
Conclusions:
- BgpA receptor overexpression creates an intracellular trap that impairs MHV replication during virion maturation and release.
- The S glycoprotein assembly or stability is specifically affected by BgpA overexpression.
- Targeting BgpA interactions could be a strategy to control MHV infections.