Evidence map›Paper›PMID 31645445›Full record

ArticleJournal of virology2020

Reverse Genetics System for a Human Group A Rotavirus.

Takahiro Kawagishi, Jeffery A Nurdin, Misa Onishi, Ryotaro Nouda, Yuta Kanai, Takeshi Tajima, Hiroshi Ushijima, Takeshi Kobayashi

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. 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
3.6field-weighted citation impact, top 6% 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, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  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

8 authors at 3 institutions in 1 country.

Takahiro Kawagishi *Department of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Jeffery A Nurdin *Department of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Misa OnishiDepartment of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Ryotaro NoudaDepartment of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Yuta KanaiDepartment of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Takeshi TajimaDepartment of Pediatrics, Hakujikai Memorial Hospital, Tokyo, Japan.
Hiroshi UshijimaDivision of Microbiology, Department of Pathology and Microbiology, Nihon University School of Medicine, Tokyo, Japan.
Takeshi KobayashiDepartment of Virology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan tkobayashi@biken.osaka-u.ac.jp.
Osaka University · JPNihon University · JPTeikyo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group A rotavirus (RV) is a major cause of acute gastroenteritis in infants and young children worldwide. Recently, we established an entirely plasmid-based reverse genetics system for simian RV strain SA11. Although that system was robust enough to generate reassortant RVs, including human RV gene segments, and enabled better understanding of the biological differences between animal and human RV strains, a complete reverse genetics system for human RV strains is desirable. Here, we established a plasmid-based reverse genetics system for G4P[8] human RV strain Odelia. This technology was used to generate a panel of monoreassortant viruses between human and simian RV strains for all of the 11 gene segments demonstrating full compatibility between human and simian RV strains. Furthermore, we generated recombinant viruses lacking the C-terminal region of the viral nonstructural protein NSP1 and used it to define the biological function of the interaction between NSP1 and its target protein β-transducin repeat-containing protein (β-TrCP) during viral replication. While the NSP1 truncation mutant lacking the C-terminal 13 amino acids displayed lower β-TrCP degradation activity, it replicated as efficiently as the wild-type virus. In contrast, the truncation mutant lacking the C-terminal 166 amino acids of NSP1 replicated poorly, suggesting that the C-terminal region of NSP1 plays critical roles in viral replication. The system reported here will allow generation of engineered recombinant virus harboring desired mutations, increase our understanding of the molecular biology of human RV, and facilitate development of novel therapeutics and vaccines.

Indexed as

MutationReverse GeneticsAnimalsbeta-Transducin Repeat-Containing ProteinsHaplorhiniHEK293 CellsHumansRotavirusRotavirus InfectionsViral Nonstructural ProteinsVirus Replicationbeta-Transducin Repeat-Containing ProteinsViral Nonstructural Proteinsreverse genetics systemrotavirusvirus-host interactions

Identifiers

PMID31645445
PMCPMC6955264
OpenAlexW2980892742

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.