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The Interaction between Nidovirales and Autophagy Components

Authors: Yingying Cong; Pauline Verlhac; Fulvio Reggiori;

The Interaction between Nidovirales and Autophagy Components

Abstract

Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruses, usurp autophagy in order to promote their propagation. Nidovirales are an order of enveloped viruses with large single-stranded positive RNA genomes. Four virus families (Arterividae, Coronaviridae, Mesoniviridae, and Roniviridae) are part of this order, which comprises several human and animal pathogens of medical and veterinary importance. In host cells, Nidovirales induce membrane rearrangements including autophagosome formation. The relevance and putative mechanism of autophagy usurpation, however, remain largely elusive. Here, we review the current knowledge about the possible interplay between Nidovirales and autophagy.

Subjects by Vocabulary

Microsoft Academic Graph classification: Autophagosome medicine.disease_cause Arterivirus Nidovirales medicine Coronaviridae Coronavirus biology Autophagy RNA biology.organism_classification Cell biology Viral replication

Library of Congress Subject Headings: lcsh:QR1-502 lcsh:Microbiology

Keywords

replication, ronivirus, coronavirus, autophagosome, Review, autophagic flux, Nidovirales, Virus Replication, arterivirus, Virology, Autophagy, Animals, Humans, Nidovirales/physiology, infection, Infectious Diseases, Host-Pathogen Interactions, egression, mesonivirus

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    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    30
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Average
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
  • citations
    This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    30
    popularity
    This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
    Top 10%
    influence
    This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
    Average
    impulse
    This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
    Top 10%
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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
30
Top 10%
Average
Top 10%
Funded by
EC| PRONKJEWAIL
Project
PRONKJEWAIL
Protecting patients with enhanced susceptibility to infections
  • Funder: European Commission (EC)
  • Project Code: 713660
  • Funding stream: H2020 | MSCA-COFUND-DP
,
SNSF| ER-phagy mechanisms to maintain and restore endoplasmic reticulum homeostasis
Project
  • Funder: Swiss National Science Foundation (SNSF)
  • Project Code: 154421
  • Funding stream: Programmes | Sinergia
iis
,
NWO| A three-dimensional look into autophagy
Project
  • Funder: Netherlands Organisation for Scientific Research (NWO) (NWO)
  • Project Code: 016.130.606
iis
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