Evidence map›Paper›PMID 24335315›Full record

ArticleJournal of virology2014

Characterization of human astrovirus cell entry.

Ernesto Méndez, Claudia Muñoz-Yañez, Claudia Sánchez-San Martín, Gabriela Aguirre-Crespo, M del Rocio Baños-Lara, Michelle Gutierrez, Rafaela Espinosa, Yunuén Acevedo, Carlos F Arias, Susana López

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Neonatal Fc receptor is a functional receptor for classical human astrovirus.Genes to cells : devoted to molecular & cellular mechanisms · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Structure of the divergent human astrovirus MLB capsid spike.Structure (London, England : 1993) · 2022
    Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
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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

10 authors at 1 institution in 1 country.

Ernesto MéndezDepartamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, Morelos, Mexico.
Claudia Muñoz-Yañez
Claudia Sánchez-San Martín
Gabriela Aguirre-Crespo
M del Rocio Baños-Lara
Michelle Gutierrez
Rafaela Espinosa
Yunuén Acevedo
Carlos F Arias
Susana López
Universidad Nacional Autónoma de México · MX

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human astroviruses (HAstV) are a frequent cause of gastroenteritis in young children and immunocompromised patients. To understand the early steps of HAstV infection in the highly permissive Caco-2 cell line, the binding and entry processes of the virus were characterized. The half-time of virus binding to the cell surface was about 10 min, while virus decapsidation took around 130 min. Drugs affecting clathrin-mediated endocytosis, endosome acidification, and actin filament polymerization, as well as those that reduce the presence of cholesterol in the cell membrane, decreased the infectivity of the virus. The infection was also reduced by silencing the expression of the clathrin heavy chain (CHC) by RNA interference or by overexpression of dominant-negative mutants of dynamin 2 and Eps15. Furthermore, the entry of HAstV apparently depends on the maturation of endosomes, since the infection was reduced by silencing the expression of Rab7, a small GTPase involved in the early- to late-endosome maturation. Altogether, our results suggest that HAstV enters Caco-2 cells using a clathrin-dependent pathway and reaches late endosomes to enter cells. Here, we have characterized the mechanism used by human astroviruses, important agents of gastroenteritis in children, to gain entry into their host cells. Using a combination of biochemical and genetic tools, we found that these viruses enter Caco-2 cells using a clathrin-dependent endocytic pathway, where they most likely need to travel to late endosomes to reach the cytoplasm and begin their replication cycle.

Indexed as

Virus InternalizationAdaptor Proteins, Vesicular TransportAntiviral AgentsAstroviridae InfectionsCell LineClathrinDynaminsEndoribonucleasesFungal ProteinsGene SilencingHumansMamastrovirusMutationrab7 GTP-Binding Proteinsrab GTP-Binding ProteinsVirus AttachmentAdaptor Proteins, Vesicular Transportalpha-sarcinAntiviral AgentsClathrinDynaminsEndoribonucleasesEPN2 protein, humanFungal Proteinsrab7 GTP-Binding Proteinsrab7 GTP-binding proteins, humanrab GTP-Binding Proteins

Identifiers

PMID24335315
PMCPMC3958088
OpenAlexW2107356426

What OpenQuestion holds

Textmetadata
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.