Mouse Norovirus infection promotes autophagy induction to facilitate replication but prevents final autophagosome maturation
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Updated: Mar 25, 2026

Reverse Genetics Mediated Recovery of Infectious Murine Norovirus
Published on: June 24, 2012
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.
Abstract:
Autophagy is a cellular process used to eliminate intracellular pathogens. Many viruses however are able to manipulate this cellular process for their own advantage. Here we demonstrate that Mouse Norovirus (MNV) infection induces autophagy but does not appear to utilise the autophagosomal membrane for establishment and formation of the viral replication complex. We have observed that MNV infection results in lipidation and recruitment of LC3 to the autophagosome membrane but prevents subsequent fusion of the autophagosomes with lysosomes, as SQSTM1 (an autophagy receptor) accumulates and Lysosome-Associated Membrane Protein1 is sequestered to the MNV replication complex (RC) rather than to autophagosomes. We have additionally observed that chemical modulation of autophagy differentially affects MNV replication. From this study we can conclude that MNV infection induces autophagy, however suppresses the final maturation step of this response, indicating that autophagy induction contributes to MNV replication independently of RC biogenesis.
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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