Mouse Norovirus infection promotes autophagy induction to facilitate replication but prevents final autophagosome

Tanya B O'Donnell1, Jennifer L Hyde2, Justine D Mintern3

  • 1Department of Microbiology and Immunology, at the Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne 3010, Australia.

Virology
|February 29, 2016
PubMed

Insights

Mouse Norovirus (MNV) induces autophagy but blocks its final maturation. This autophagy induction aids MNV replication, independent of viral replication complex formation.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Autophagy is a cellular defense mechanism against intracellular pathogens.
  • Viruses often exploit host cell processes, including autophagy, for their own replication.

Purpose of the Study:

  • To investigate the role of autophagy in Mouse Norovirus (MNV) infection.
  • To determine if MNV utilizes the autophagosomal pathway for replication complex formation.

Main Methods:

  • Monitoring autophagy markers (LC3 lipidation, SQSTM1 accumulation) during MNV infection.
  • Assessing the localization of Lysosome-Associated Membrane Protein1.
  • Evaluating the impact of chemical autophagy modulation on MNV replication.

Main Results:

  • MNV infection induces autophagy, marked by LC3 recruitment to autophagosomes.
  • MNV inhibits autophagosome-lysosome fusion, leading to SQSTM1 accumulation.
  • Lysosome-Associated Membrane Protein1 is sequestered to the MNV replication complex.
  • Chemical modulation of autophagy affects MNV replication.

Conclusions:

  • MNV induces autophagy but suppresses its maturation.
  • Autophagy contributes to MNV replication independently of replication complex biogenesis.

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