Unconventional use of LC3 by coronaviruses through the alleged subversion of the ERAD tuning pathway

Viruses. 2011 Sep;3(9):1610-23. doi: 10.3390/v3091610. Epub 2011 Sep 5.

Abstract

Pathogens of bacterial and viral origin hijack pathways operating in eukaryotic cells in many ways in order to gain access into the host, to establish themselves and to eventually produce their progeny. The detailed molecular characterization of the subversion mechanisms devised by pathogens to infect host cells is crucial to generate targets for therapeutic intervention. Here we review recent data indicating that coronaviruses probably co-opt membranous carriers derived from the endoplasmic reticulum, which contain proteins that regulate disposal of misfolded polypeptides, for their replication. In addition, we also present models describing potential mechanisms that coronaviruses could employ for this hijacking.

Keywords: EDEM1; EDEMosomes; ER quality control; ERAD; MHV; OS-9; SARS-coronavirus; autophagy; coronaviruses; double-membrane vesicles; nidoviruses.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Autophagy / physiology
  • Coronaviridae / physiology*
  • Coronaviridae Infections / virology
  • Endoplasmic Reticulum / metabolism
  • Endoplasmic Reticulum / virology*
  • Endoplasmic Reticulum-Associated Degradation*
  • Humans
  • Mammals / metabolism*
  • Membrane Proteins / metabolism
  • Mice
  • Microtubule-Associated Proteins / metabolism
  • Models, Biological
  • Transport Vesicles / metabolism
  • Transport Vesicles / virology*
  • Virus Replication*

Substances

  • MAP1LC3A protein, human
  • Membrane Proteins
  • Microtubule-Associated Proteins