Evidence map›Paper›PMID 26334635›Full record

ArticlePLoS pathogens2015

Inhibition of Translation Initiation by Protein 169: A Vaccinia Virus Strategy to Suppress Innate and Adaptive Immunity and Alter Virus Virulence.

Pavla Strnadova, Hongwei Ren, Robert Valentine, Michela Mazzon, Trevor R Sweeney, Ian Brierley, Geoffrey L Smith

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Ribosomes in poxvirus infection.Current opinion in virology · 2022
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Translational control during poxvirus infection.Wiley interdisciplinary reviews. RNA · 2019
    Review
  17. Article
  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

7 authors at 2 institutions in 1 country.

Pavla StrnadovaDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom; Department of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Hongwei RenDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom; Department of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Robert ValentineDepartment of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Michela MazzonDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom; Department of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
Trevor R SweeneyDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Ian BrierleyDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom.
Geoffrey L SmithDepartment of Pathology, University of Cambridge, Cambridge, United Kingdom; Department of Virology, Faculty of Medicine, Imperial College London, London, United Kingdom.
University of Cambridge · GBImperial College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G008205/1Medical Research Council G0800151Medical Research Council MR/M011747/1Wellcome TrustWellcome Trust 090315
6 · The paper itself

Abstract

Vaccinia virus (VACV) is the prototypic orthopoxvirus and the vaccine used to eradicate smallpox. Here we show that VACV strain Western Reserve protein 169 is a cytoplasmic polypeptide expressed early during infection that is excluded from virus factories and inhibits the initiation of cap-dependent and cap-independent translation. Ectopic expression of protein 169 causes the accumulation of 80S ribosomes, a reduction of polysomes, and inhibition of protein expression deriving from activation of multiple innate immune signaling pathways. A virus lacking 169 (vΔ169) replicates and spreads normally in cell culture but is more virulent than parental and revertant control viruses in intranasal and intradermal murine models of infection. Intranasal infection by vΔ169 caused increased pro-inflammatory cytokines and chemokines, infiltration of pulmonary leukocytes, and lung weight. These alterations in innate immunity resulted in a stronger CD8+ T-cell memory response and better protection against virus challenge. This work illustrates how inhibition of host protein synthesis can be a strategy for virus suppression of innate and adaptive immunity.

Indexed as

Adaptive ImmunityHost-Pathogen InteractionsImmunity, InnatePeptide Chain Initiation, TranslationalAnimalsCD8-Positive T-LymphocytesCell LineFemaleGene DeletionGene Expression RegulationHumansImmunologic MemoryMice, Inbred BALB CMice, Inbred C57BLRecombinant Fusion ProteinsRecombinant ProteinsRecombinant Fusion ProteinsRecombinant ProteinsViral Proteins

Identifiers

PMID26334635
PMCPMC4559412
OpenAlexW1784712937

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.