Evidence map›Paper›PMID 22423969›Full record

ArticleCell host & microbe2012

Pancreatic acinar cell-specific autophagy disruption reduces coxsackievirus replication and pathogenesis in vivo.

Mehrdad Alirezaei, Claudia T Flynn, Malcolm R Wood, J Lindsay Whitton

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 3% of its field
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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 80 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Viruses and autophagy: bend, but don't break.Nature reviews. Microbiology · 2024
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Advances in cell death mechanisms involved in viral myocarditis.Frontiers in cardiovascular medicine · 2022
    Review
  14. Moments in autophagy and disease: Past and present.Molecular aspects of medicine · 2021
    Review
  15. Autophagy in major human diseases.The EMBO journal · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Autophagy and microbial pathogenesis.Cell death and differentiation · 2020
    Review
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

4 authors at 1 institution in 1 country.

Mehrdad AlirezaeiDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.
Claudia T Flynn
Malcolm R Wood
J Lindsay Whitton
Scripps Research Institute · US

Funding

COXSACKIE MYOCARDITIS AND VIRAL PERSISTENCE IN THE HEARTR01AI042314 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI WHITTON, J. LINDSAY · 1998 to 2013
$5.6M
Innate and Adaptive Immune Responses in the Virus-Infected HeartR01HL093177 · NHLBI · SCRIPPS RESEARCH INSTITUTE, THE · PI WHITTON, J. LINDSAY · 2010 to 2013
$1.9M
NHLBI NIH HHS R01 HL093177NIAID NIH HHS R01 AI042314
6 · The paper itself

Abstract

Autophagy protects against many infections by inducing the lysosomal-mediated degradation of invading pathogens. However, previous in vitro studies suggest that some enteroviruses not only evade these protective effects but also exploit autophagy to facilitate their replication. We generated Atg5(f/f)/Cre(+) mice, in which the essential autophagy gene Atg5 is specifically deleted in pancreatic acinar cells, and show that coxsackievirus B3 (CVB3) requires autophagy for optimal infection and pathogenesis. Compared to Cre(-) littermates, Atg5(f/f)/Cre(+) mice had an ∼2,000-fold lower CVB3 titer in the pancreas, and pancreatic pathology was greatly diminished. Both in vivo and in vitro, Atg5(f/f)/Cre(+) acinar cells had reduced intracellular viral RNA and proteins. Furthermore, intracellular structural elements induced upon CVB3 infection, such as compound membrane vesicles and highly geometric paracrystalline arrays, which may represent viral replication platforms, were infrequently observed in infected Atg5(f/f)/Cre(+) cells. Thus, CVB3-induced subversion of autophagy not only benefits the virus but also exacerbates pancreatic pathology.

Indexed as

AutophagyVirus ReplicationAcinar CellsAnimalsAutophagy-Related Protein 5Coxsackievirus InfectionsEnterovirusHost-Pathogen InteractionsMiceMice, TransgenicMicrotubule-Associated ProteinsPancreasSignal TransductionAtg5 protein, mouseAutophagy-Related Protein 5Microtubule-Associated Proteins

Identifiers

PMID22423969
PMCPMC3308121
OpenAlexW2060522415

What OpenQuestion holds

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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.