Evidence map›Paper›PMID 19587035›Full record

ArticleJournal of virology2009

Insight into poliovirus genome replication and encapsidation obtained from studies of 3B-3C cleavage site mutants.

Hyung Suk Oh, Harsh B Pathak, Ian G Goodfellow, Jamie J Arnold, Craig E Cameron

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Non-lytic spread of poliovirus requires the nonstructural protein 3CD.bioRxiv : the preprint server for biology · 2024
    Article
  5. An efficientJournal of virology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Functional advantages of triplication of the 3B coding region of the FMDV genome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Allosteric inhibitors of Coxsackie virus A24 RNA polymerase.Bioorganic & medicinal chemistry · 2016
    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

5 authors at 2 institutions in 2 countries.

Hyung Suk OhDepartment of Biochemistry and Molecular Biology, Pennsylvania State University, University Park, 16802, USA.
Harsh B Pathak
Ian G Goodfellow
Jamie J Arnold
Craig E Cameron
Pennsylvania State University · USImperial College London · GB

Funding

Picornavirus Genome ReplicationR01AI053531 · NIAID · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI CAMERON, CRAIG E. · 2003 to 2017
$5.7M
Picornavirus Genome ReplicationR37AI053531 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CRAIG E. CAMERON · 2018 to 2026
$4.8M
Picornavirus Genome ReplicationR56AI053531 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI CAMERON, CRAIG E. · 2008 to 2008
$439k
NIAID NIH HHS AI053531NIAID NIH HHS R01 AI053531NIAID NIH HHS R37 AI053531NIAID NIH HHS R56 AI053531Wellcome Trust 081624
6 · The paper itself

Abstract

A poliovirus (PV) mutant (termed GG), which is incapable of producing 3AB, VPg, and 3CD proteins due to a defective cleavage site between the 3B and 3C proteins, replicated, producing 3BC-linked RNA rather than the VPg-linked RNA produced by the wild type (WT). GG PV RNA is quasi-infectious. The yield of infectious GG PV relative to replicated RNA is reduced by almost 5 logs relative to that of WT PV. Proteolytic activity required for polyprotein processing is normal for the GG mutant. 3BC-linked RNA can be encapsidated as efficiently as VPg-linked RNA. However, a step after genome replication but preceding virus assembly that is dependent on 3CD and/or 3AB proteins limits production of infectious GG PV. This step may involve release of replicated genomes from replication complexes. A pseudorevertant (termed EG) partially restored cleavage at the 3B-3C cleavage site. The reduced rate of formation of 3AB and 3CD caused corresponding reductions in the observed rate of genome replication and infectious virus production by EG PV without impacting the final yield of replicated RNA or infectious virus relative to that of WT PV. Using EG PV, we showed that genome replication and encapsidation were distinct steps in the multiplication cycle. Ectopic expression of 3CD protein reversed the genome replication phenotype without alleviating the infectious-virus production phenotype. This is the first report of a trans-complementable function for 3CD for any picornavirus. This observation supports an interaction between 3CD protein and viral and/or host factors that is critical for genome replication, perhaps formation of replication complexes.

Indexed as

Genome, ViralVirus AssemblyHumansMutationPoliovirusPolyproteinsRNA, ViralViral ProteinsVirus ReplicationPolyproteinsRNA, ViralViral Proteins

Identifiers

PMID19587035
PMCPMC2738245
OpenAlexW2081913826

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.