Evidence map›Paper›PMID 34948268›Full record

ReviewInternational journal of molecular sciences2021

The Role of Host Glycobiology and Gut Microbiota in Rotavirus and Norovirus Infection, an Update.

Nazaret Peña-Gil, Cristina Santiso-Bellón, Roberto Gozalbo-Rovira, Javier Buesa, Vicente Monedero, Jesús Rodríguez-Díaz

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Gut microbes · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Non-Secretor Status Due toMicroorganisms · 2025
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 2 institutions in 1 country.

Nazaret Peña-GilDepartment of Microbiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.
Cristina Santiso-BellónDepartment of Microbiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.ORCID 0000-0003-1698-5062
Roberto Gozalbo-RoviraDepartment of Microbiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.ORCID 0000-0003-3427-3800
Javier BuesaDepartment of Microbiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.ORCID 0000-0002-3328-3428
Vicente MonederoDepartment of Biotechnology, Institute of Agrochemistry and Food Technology (IATA-CSIC), 46980 Paterna, Spain.
Jesús Rodríguez-DíazDepartment of Microbiology, School of Medicine, University of Valencia, Avda. Blasco Ibáñez 17, 46010 Valencia, Spain.ORCID 0000-0002-9698-7684
Universitat de València · ESInstituto de Agroquímica y Tecnología de Alimentos · ES

Funding

Generalitat Valenciana IDIFEDER/2018/056Ministry of Economy, Industry and Competitiveness AGL2017-84165-C2-2-R and PID2020-115403RB-C22
6 · The paper itself

Abstract

Rotavirus (RV) and norovirus (NoV) are the leading causes of acute gastroenteritis (AGE) worldwide. Several studies have demonstrated that histo-blood group antigens (HBGAs) have a role in NoV and RV infections since their presence on the gut epithelial surfaces is essential for the susceptibility to many NoV and RV genotypes. Polymorphisms in genes that code for enzymes required for HBGAs synthesis lead to secretor or non-secretor and Lewis positive or Lewis negative individuals. While secretor individuals appear to be more susceptible to RV infections, regarding NoVs infections, there are too many discrepancies that prevent the ability to draw conclusions. A second factor that influences enteric viral infections is the gut microbiota of the host. In vitro and animal studies have determined that the gut microbiota limits, but in some cases enhances enteric viral infection. The ways that microbiota can enhance NoV or RV infection include virion stabilization and promotion of virus attachment to host cells, whereas experiments with microbiota-depleted and germ-free animals point to immunoregulation as the mechanism by which the microbiota restrict infection. Human trials with live, attenuated RV vaccines and analysis of the microbiota in responder and non-responder individuals also allowed the identification of bacterial taxa linked to vaccine efficacy. As more information is gained on the complex relationships that are established between the host (glycobiology and immune system), the gut microbiota and intestinal viruses, new avenues will open for the development of novel anti-NoV and anti-RV therapies.

Indexed as

AnimalsBlood Group AntigensCaliciviridae InfectionsGastroenteritisGastrointestinal MicrobiomeGenotypeGlycomicsHumansImmunityNorovirusRotavirusRotavirus InfectionsVaccine EfficacyViral VaccinesBlood Group AntigensViral Vaccinesgut microbiotaHBGAsnorovirusrotavirus

Identifiers

PMID34948268
PMCPMC8704558
OpenAlexW4200319538

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.