Evidence map›Paper›PMID 9696817›Full record

ArticleJournal of virology1998

Rotavirus infection reduces sucrase-isomaltase expression in human intestinal epithelial cells by perturbing protein targeting and organization of microvillar cytoskeleton.

N Jourdan, J P Brunet, C Sapin, A Blais, J Cotte-Laffitte, F Forestier, A M Quero, G Trugnan, A L Servin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.1field-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

52 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
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  4. Frontiers in cell and developmental biology · 2021
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  6. Review
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  11. Glucose enhances rotavirus enterotoxin-induced intestinal chloride secretion.Pflugers Archiv : European journal of physiology · 2017
    Article
  12. Article
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  15. Pathogen-induced secretory diarrhea and its prevention.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2016
    Review
  16. Diversity in Rotavirus-Host Glycan Interactions: A "Sweet" Spectrum.Cellular and molecular gastroenterology and hepatology · 2016
    Review
  17. Article
  18. Article
  19. Article
  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 at 4 institutions in 1 country.

N JourdanInstitut National de la Santé et de la Recherche Médicale, CJF 94 07, Pathogénie Cellulaire et Moléculaire des Microorganismes Entérovirulents, Faculté de Pharmacie, Université Paris XI, 92296 Chatenay-Malabry Cedex, France.
J P Brunet
C Sapin
A Blais
J Cotte-Laffitte
F Forestier
A M Quero
G Trugnan
A L Servin
Université Paris-Saclay · FRInserm · FRSorbonne Université · FRToxicologie, Pharmacologie et Signalisation Cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rotavirus infection is the most common cause of severe infantile gastroenteritis worldwide. These viruses infect mature enterocytes of the small intestine and cause structural and functional damage, including a reduction in disaccharidase activity. It was previously hypothesized that reduced disaccharidase activity resulted from the destruction of rotavirus-infected enterocytes at the villus tips. However, this pathophysiological model cannot explain situations in which low disaccharidase activity is observed when rotavirus-infected intestine exhibits few, if any, histopathologic changes. In a previous study, we demonstrated that the simian rotavirus strain RRV replicated in and was released from human enterocyte-like Caco-2 cells without cell destruction (N. Jourdan, M. Maurice, D. Delautier, A. M. Quero, A. L. Servin, and G. Trugnan, J. Virol. 71:8268-8278, 1997). In the present study, to reinvestigate disaccharidase expression during rotavirus infection, we studied sucrase-isomaltase (SI) in RRV-infected Caco-2 cells. We showed that SI activity and apical expression were specifically and selectively decreased by RRV infection without apparent cell destruction. Using pulse-chase experiments and cell surface biotinylation, we demonstrated that RRV infection did not affect SI biosynthesis, maturation, or stability but induced the blockade of SI transport to the brush border. Using confocal laser scanning microscopy, we showed that RRV infection induces important alterations of the cytoskeleton that correlate with decreased SI apical surface expression. These results lead us to propose an alternate model to explain the pathophysiology associated with rotavirus infection.

Indexed as

Biological TransportCaco-2 CellsCell MembraneCytoskeletonHumansIntestinal MucosaMicrovilliRotavirusSucrase-Isomaltase ComplexSucrase-Isomaltase Complex

Identifiers

PMID9696817
PMCPMC109945
OpenAlexW1752632498

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.