Evidence map›Paper›PMID 19515769›Full record

ArticleJournal of virology2009

Fate of minus-strand templates and replication complexes produced by a p23-cleavage-defective mutant of Sindbis virus.

Junbo Mai, Stanley G Sawicki, Dorothea L Sawicki

Abstract 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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

  1. Antagonism of RNA silencing in the yellow fever mosquito,Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. A robust fluorogenic substrate for chikungunya virus protease (nsP2) activity.Protein science : a publication of the Protein Society · 2025
    Article
  3. Article
  4. Molecular Virology of Chikungunya Virus.Current topics in microbiology and immunology · 2022
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
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.

Junbo MaiDepartment of Medical Microbiology and Immunology, University of Toledo College of Medicine, Health Science Campus, 3000 Arlington Avenue, Toledo, OH 43614, USA.
Stanley G Sawicki
Dorothea L Sawicki
University of Toledo Medical Center · US

Funding

Alphavirus Minus Strand RNA Synthesis and RNase LR01AI057571 · NIAID · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI SAWICKI, DOROTHEA L · 2005 to 2009
$1.4M
NIAID NIH HHS AI057571NIAID NIH HHS R01 AI057571
6 · The paper itself

Abstract

SIN2V is an engineered mutant Sindbis virus (SIN) that is unable to process the P23 cleavage site in polyproteins P123 and P1234 that are translated from the genome after its entry into cells. Unlike wild-type (wt) SIN, it caused minus strands to be made continuously and replication-transcription complex (RTC) activity to be unstable (R. Gorchakov, E. Frolova, S. Sawicki, S. Atasheva, D. Sawicki, and I. Frolov, J. Virol. 82:6218-6231, 2008). We examined further the effects of P23 on SIN RNA replication and RTC activity. Continuous minus-strand synthesis by SIN2V produced 250% of wt levels of minus strands but accumulated only 110% of wt levels (0.39 pg, or 2.7 x 10(4) molecules of double-stranded RNA per cell). Because SIN2V-infected cells accumulated only 40% of the minus strands that were made, cells must possess some process to limit RTC accumulation. The loss of activity by SIN2V RTC after translation was inhibited was stochastic and not due to their inherent instability, based on finding that activity was lost without the degradation of the minus-strand templates. In addition to their normal functions, P23 RTCs exhibited the novel phenotype of being unable to switch from making less to making more genomes than subgenomic 26S mRNA at late times during infections. Our results lend credence to the hypothesis that nsP2 (and possibly nsP3) possesses functions other than those needed solely for RTC activity and that it may also act with the host to regulate minus-strand synthesis and the stability of the RTC.

Indexed as

Virus ReplicationCysteine EndopeptidasesModels, BiologicalPolyproteinsProtein Processing, Post-TranslationalRNA StabilityRNA, ViralSindbis VirusViral Nonstructural ProteinsCysteine EndopeptidasesnsP2 proteinasensp3 protein, alphavirusPolyproteinsRNA, ViralViral Nonstructural Proteins

Identifiers

PMID19515769
PMCPMC2738138
OpenAlexW2147642616

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.