Evidence map›Paper›PMID 19656875›Full record

ArticleJournal of virology2009

Venezuelan equine encephalitis virus disrupts STAT1 signaling by distinct mechanisms independent of host shutoff.

Jason D Simmons, Laura J White, Thomas E Morrison, Stephanie A Montgomery, Alan C Whitmore, Robert E Johnston, Mark T Heise

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 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.0field-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

59 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Microbiology spectrum · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. 3CVirologica Sinica · 2023
    Article
  13. Mechanism of Immune Evasion in Mosquito-Borne Diseases.Pathogens (Basel, Switzerland) · 2023
    Review
  14. Review
  15. Self-amplifying mRNA-Based Vaccine Technology and Its Mode of Action.Current topics in microbiology and immunology · 2022
    Article
  16. Innate immune evasion by alphaviruses.Frontiers in immunology · 2022
    Review
  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

7 authors at 2 institutions in 1 country.

Jason D SimmonsDepartment of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
Laura J White
Thomas E Morrison
Stephanie A Montgomery
Alan C Whitmore
Robert E Johnston
Mark T Heise
University of North Carolina at Chapel Hill · USUniversity of Colorado Denver · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM008719 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI DARVILLE, TONI, DESHMUKH, MOHANISH P · 1999 to 2023
$15.1M
Molecular Biology of Viral Diseases Predoctoral Training GrantT32AI007419 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Mark T Heise, CARY A MOODY · 1993 to 2026
$4.7M
Immune Evasion Mechanisms of Neurovirulent AlphavirusesR01AI067641 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HEISE, MARK T · 2008 to 2012
$1.4M
NIAID NIH HHS R01 AI067641NIAID NIH HHS T32 AI007419NIGMS NIH HHS T32 GM008719
6 · The paper itself

Abstract

Venezuelan equine encephalitis virus (VEEV) is an important human and veterinary pathogen causing sporadic epizootic outbreaks of potentially fatal encephalitis. The type I interferon (IFN) system plays a central role in controlling VEEV and other alphavirus infections, and IFN evasion is likely an important determinant of whether these viruses disseminate and cause disease within their hosts. Alphaviruses are thought to limit the induction of type I IFNs and IFN-stimulated genes by shutting off host cell macromolecular synthesis, which in the case of VEEV is partially mediated by the viral capsid protein. However, more specific strategies by which alphaviruses inhibit type I IFN signaling have not been characterized. Analyses of cells infected with VEEV and VEEV replicon particles (VRP) demonstrate that viral infection rapidly disrupts tyrosine phosphorylation and nuclear translocation of the transcription factor STAT1 in response to both IFN-beta and IFN-gamma. This effect was independent of host shutoff and expression of viral capsid, suggesting that VEEV uses novel mechanisms to interfere with type I and type II IFN signaling. Furthermore, at times when STAT1 activation was efficiently inhibited, VRP infection did not limit tyrosine phosphorylation of Jak1, Tyk2, or STAT2 after IFN-beta treatment but did inhibit Jak1 and Jak2 activation in response to IFN-gamma, suggesting that VEEV interferes with STAT1 activation by the type I and II receptor complexes through distinct mechanisms. Identification of the viral requirements for this novel STAT1 inhibition will further our understanding of alphavirus molecular pathogenesis and may provide insights into effective alphavirus-based vaccine design.

Indexed as

Signal TransductionAnimalsChlorocebus aethiopsCricetinaeEncephalitis Virus, Venezuelan EquineHeLa CellsHumansInterferon-betaInterferon-gammaPhosphorylationSTAT1 Transcription FactorTyrosineVero CellsInterferon-betaInterferon-gammaSTAT1 protein, humanSTAT1 Transcription FactorTyrosine

Identifiers

PMID19656875
PMCPMC2753124
OpenAlexW2130397544

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.