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Related Experiment Videos

Coronavirus replication complex formation utilizes components of cellular autophagy.

Erik Prentice1, W Gray Jerome, Tamotsu Yoshimori

  • 1Department of Microbiology and Immunology, Elizabeth B. Lamb Center for Pediatric Research, Vanderbilt University Medical Center, Nashville, Tennessee 37221, USA.

The Journal of Biological Chemistry
|December 31, 2003
PubMed
Summary

Autophagy is essential for mouse hepatitis virus (MHV) replication, enabling the formation of double-membrane vesicles (DMVs) required for RNA synthesis. This process enhances viral replication efficiency.

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Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Mouse hepatitis virus (MHV) replicates RNA within double-membrane vesicles (DMVs) in host cell cytoplasm.
  • The biogenesis of these DMVs during MHV infection remains poorly understood.

Purpose of the Study:

  • To investigate the role of autophagy in the formation of DMVs.
  • To determine the impact of autophagy on MHV replication.

Main Methods:

  • Genetic manipulation of autophagy-related genes (e.g., APG5 knockout).
  • Biochemical assays to detect viral replication complexes.
  • Cell imaging techniques to visualize DMVs and protein localization.

Main Results:

  • Autophagy proteins (LC3, Apg12) co-localized with MHV replication complexes.

Related Experiment Videos

  • MHV infection induced autophagy via a 3-methyladenine-resistant pathway.
  • APG5 knockout cells showed impaired MHV replication and lacked DMVs, with swollen rough endoplasmic reticulum instead.
  • Restoring Apg5 expression in knockout cells rescued MHV replication.

    • Conclusions:

    • Autophagy is a critical host factor required for the formation of double-membrane-bound MHV replication complexes.
    • DMV formation, facilitated by autophagy, significantly enhances MHV replication efficiency.
    • The rough endoplasmic reticulum is suggested as the membrane source for replication complexes.