Evidence map›Paper›PMID 28531150›Full record

ArticleViruses2017

Distinct Contributions of Autophagy Receptors in Measles Virus Replication.

Denitsa S Petkova, Pauline Verlhac, Aurore Rozières, Joël Baguet, Mathieu Claviere, Carole Kretz-Remy, Renaud Mahieux, Christophe Viret, Mathias Faure

Abstract read
In one paragraph

Article in Viruses, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Guideline
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Autophagy receptors as viral targets.Cellular & molecular biology letters · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. The Role of Autophagy and Autophagy Receptor NDP52 in Microbial Infections.International journal of molecular sciences · 2020
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Denitsa S PetkovaCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. denitsa.petkova8@gmail.com.
Pauline VerlhacCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. pverlhac@gmail.com.
Aurore RozièresCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. aurore.rozieres@inserm.fr.
Joël BaguetCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. joel.baguet@inserm.fr.
Mathieu ClaviereCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. mathieu.claviere@inserm.fr.
Carole Kretz-RemyInstitut NeuroMyoGène, CNRS UMR5310, INSERM U1217, Université Lyon 1, F-69622 Villeurbanne, France; Université de Lyon, Lyon France. carole.kretz@univ-lyon1.fr.
Renaud MahieuxCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. renaud.mahieux@ens-lyon.fr.
Christophe ViretCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. christophe.viret@inserm.fr.
Mathias FaureCIRI, International Center for Infectiology Research, Université de Lyon, 69007 Lyon, France. mathias.faure@inserm.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is a potent cell autonomous defense mechanism that engages the lysosomal pathway to fight intracellular pathogens. Several autophagy receptors can recognize invading pathogens in order to target them towards autophagy for their degradation after the fusion of pathogen-containing autophagosomes with lysosomes. However, numerous intracellular pathogens can avoid or exploit autophagy, among which is measles virus (MeV). This virus induces a complete autophagy flux, which is required to improve viral replication. We therefore asked how measles virus interferes with autophagy receptors during the course of infection. We report that in addition to NDP52/CALCOCO₂ and OPTINEURIN/OPTN, another autophagy receptor, namely T6BP/TAXIBP1, also regulates the maturation of autophagosomes by promoting their fusion with lysosomes, independently of any infection. Surprisingly, only two of these receptors, NDP52 and T6BP, impacted measles virus replication, although independently, and possibly through physical interaction with MeV proteins. Thus, our results suggest that a restricted set of autophagosomes is selectively exploited by measles virus to replicate in the course of infection.

Indexed as

AutophagyCarrier ProteinsCell Cycle ProteinsHeLa CellsHost-Pathogen InteractionsHumansIntracellular Signaling Peptides and ProteinsLysosomesMeaslesMeasles virusMembrane Transport ProteinsNeoplasm ProteinsNuclear ProteinsPhagosomesTranscription Factor TFIIIAViral ProteinsCALCOCO2 protein, humanCarrier ProteinsCell Cycle ProteinsIntracellular Signaling Peptides and ProteinsMembrane Transport ProteinsNeoplasm ProteinsNuclear ProteinsOPTN protein, humanTAX1BP1 protein, humanTranscription Factor TFIIIAViral Proteinsautophagosomeautophagy receptormaturationmeasles virus

Identifiers

PMID28531150
PMCPMC5454435

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.