Evidence map›Paper›PMID 27712623›Full record

ReviewAdvances in virus research2016

Viral and Cellular mRNA Translation in Coronavirus-Infected Cells.

K Nakagawa, K G Lokugamage, S Makino

Open access · greenAbstract readReview
In one paragraph

Review in Advances in virus research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 2 pooled it
4.6field-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

119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 239 citations in OpenAlex.

  1. Epidemiology and Etiopathogeny of COVID-19.Advances in experimental medicine and biology · 2021
    Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Innate immune evasion strategies of SARS-CoV-2.Nature reviews. Microbiology · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Article

59 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

K NakagawaThe University of Texas Medical Branch, Galveston, TX, United States.
K G LokugamageThe University of Texas Medical Branch, Galveston, TX, United States.
S MakinoThe University of Texas Medical Branch, Galveston, TX, United States; Center for Biodefense and Emerging Infectious Diseases, The University of Texas Medical Branch, Galveston, TX, United States; UTMB Center for Tropical Diseases, The University of Texas Medical Branch, Galveston, TX, United States; Sealy Center for Vaccine Development, The University of Texas Medical Branch, Galveston, TX, United States; Institute for Human Infections and Immunity, The University of Texas Medical Branch, Galveston, TX, United States. Electronic address: shmakino@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

New Paradigm for Host and Viral Gene Regulation by MERS Coronavirus nsp1R01AI114657 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2015 to 2019
$2.1M
Analysis of Coronavirus-Host Cell InteractionsR01AI099107 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI MAKINO, SHINJI · 2012 to 2016
$2.0M
NIAID NIH HHS R01 AI099107NIAID NIH HHS R01 AI114657
6 · The paper itself

Abstract

Coronaviruses have large positive-strand RNA genomes that are 5' capped and 3' polyadenylated. The 5'-terminal two-thirds of the genome contain two open reading frames (ORFs), 1a and 1b, that together make up the viral replicase gene and encode two large polyproteins that are processed by viral proteases into 15-16 nonstructural proteins, most of them being involved in viral RNA synthesis. ORFs located in the 3'-terminal one-third of the genome encode structural and accessory proteins and are expressed from a set of 5' leader-containing subgenomic mRNAs that are synthesized by a process called discontinuous transcription. Coronavirus protein synthesis not only involves cap-dependent translation mechanisms but also employs regulatory mechanisms, such as ribosomal frameshifting. Coronavirus replication is known to affect cellular translation, involving activation of stress-induced signaling pathways, and employing viral proteins that affect cellular mRNA translation and RNA stability. This chapter describes our current understanding of the mechanisms involved in coronavirus mRNA translation and changes in host mRNA translation observed in coronavirus-infected cells.

Indexed as

Genome, ViralProtein BiosynthesisAnimalsCoronavirusCoronavirus InfectionsEpithelial CellsHost-Pathogen InteractionsHumansNucleotidyltransferasesOpen Reading FramesRibosomesRNA, MessengerRNA, ViralViral Structural ProteinsNucleotidyltransferasesRNA, MessengerRNA, ViralViral Structural ProteinsCoronavirusesHost gene expressionHost shutoffRibosomal frameshiftStress responseTranslationViral gene expression

Identifiers

PMID27712623
PMCPMC5388242
OpenAlexW2518706921

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.