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Coronaviruses Hijack the LC3-I-positive EDEMosomes, ER-derived vesicles exporting short-lived ERAD regulators, for

Fulvio Reggiori1, Iryna Monastyrska, Monique H Verheije

  • 1Department of Cell Biology, University Medical Centre Utrecht, 3584 CX Utrecht, The Netherlands. f.reggiori@umcutrecht.nl

Cell Host & Microbe
|June 15, 2010
PubMed

Insights

Coronaviruses hijack host cell machinery to create replication membranes, utilizing EDEM1 for double-membrane vesicle formation. This process is independent of host cell autophagy but relies on nonlipidated LC3-I.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Coronaviruses (CoVs) are RNA viruses that induce double-membrane vesicles (DMVs) for replication.
  • The origin of membranes for CoV-induced DMVs remains unclear, as they lack conventional endoplasmic reticulum (ER) or Golgi markers.

Purpose of the Study:

  • To investigate the host cellular pathways co-opted by mouse hepatitis virus (MHV) for DMV biogenesis.
  • To elucidate the role of EDEM1 and LC3 in CoV replication.

Main Methods:

  • MHV infection of host cells.
  • Analysis of EDEM1, OS-9, and LC3 localization and function.
  • Assessment of viral replication upon LC3 downregulation or autophagy inactivation.

Main Results:

  • MHV infection leads to the accumulation of EDEM1 and OS-9 in DMVs.
  • EDEM1 is exported from the ER via a COPII-independent pathway to supply DMV membranes.
  • DMVs are coated with nonlipidated LC3/Atg8.
  • LC3 downregulation, but not autophagy inactivation, protects cells from CoV infection.

Conclusions:

  • MHV hijacks a COPII-independent ER export pathway for EDEM1 to generate replication membranes.
  • Nonlipidated LC3-I plays an autophagy-independent role in CoV infection.

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