Evidence map›Paper›PMID 17267491›Full record

ArticleJournal of virology2007

Capsid protein of eastern equine encephalitis virus inhibits host cell gene expression.

Patricia V Aguilar, Scott C Weaver, Christopher F Basler

Abstract read
In one paragraph

Article in Journal of virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
10.4field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 95 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Rational design of self-amplifying virus-like vesicles with Ebola virus glycoprotein as vaccines.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Eastern Equine Encephalitis Virus: A Scoping Review of the Global Evidence.Vector borne and zoonotic diseases (Larchmont, N.Y.) · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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 2 institutions in 2 countries.

Patricia V AguilarDepartment of Microbiology, Box 1124, Mount Sinai School of Medicine, 1 Gustave L. Levy Place, New York, NY 10029, USA.
Scott C Weaver
Christopher F Basler
Icahn School of Medicine at Mount Sinai · USThe University of Texas Medical Branch at Galveston · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LIPKIN, W. IAN · 2003 to 2014
$100.8M
NIAID NIH HHS AI057158NIAID NIH HHS U54 AI057158
6 · The paper itself

Abstract

Eastern equine encephalitis virus (EEEV) causes sporadic but often severe cases of human and equine neurological disease in North America. To determine how EEEV may evade innate immune responses, we screened individual EEEV proteins for the ability to rescue the growth of a Newcastle disease virus expressing green fluorescent protein (NDV-GFP) from the antiviral effects of interferon (IFN). Only expression of the EEEV capsid facilitated NDV-GFP replication. Inhibition of the antiviral effects of IFN by the capsid appears to occur through a general inhibition of cellular gene expression. For example, the capsid inhibited the expression of several reporter genes under the control of RNA polymerase II promoters. In contrast, capsid did not inhibit expression from a T7 RNA polymerase promoter construct, suggesting that the inhibition of gene expression is specific and is not a simple manifestation of toxicity. The inhibition correlated both with capsid-induced phosphorylation of eukaryotic initiation factor 2 alpha and with capsid-mediated inhibition of cellular mRNA accumulation. Mapping analysis identified the N terminus as the region important for the inhibition of host gene expression, suggesting that this inhibition is independent of capsid protease activity. Finally, when cell lines containing EEEV replicons encoding capsid were selected, replicons consistently acquired mutations that deleted all or part of the capsid, for example, amino acids 18 to 135. Given that the amino terminus of the capsid is required to inhibit host cell gene expression, these data suggest that capsid expression from the replicons is ultimately toxic to host cells, presumably because of its ability to inhibit gene expression.

Indexed as

Gene Expression RegulationCapsid ProteinsCell LineChloramphenicol O-AcetyltransferaseEncephalitis Virus, Eastern EquineEukaryotic Initiation Factor-2Genes, ReporterGreen Fluorescent ProteinsHumansInterferon-gammaLuciferasesPhosphorylationProtein Structure, TertiaryRNA, MessengerVirus ReplicationCapsid ProteinsChloramphenicol O-Acetyltransferaseenhanced green fluorescent proteinEukaryotic Initiation Factor-2Green Fluorescent ProteinsInterferon-gammaLuciferasesRNA, Messenger

Identifiers

PMID17267491
PMCPMC1866141
OpenAlexW2001826761

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.