Evidence map›Paper›PMID 24265839›Full record

ArticlePloS one2013

Agnogene deletion in a novel pathogenic JC virus isolate impairs VP1 expression and virion production.

Laura C Ellis, Elizabeth Norton, Xin Dang, Igor J Koralnik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. 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
1.7field-weighted citation impact, top 15% 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, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. JC Virus Infects Neurons and Glial Cells in the Hippocampus.Journal of neuropathology and experimental neurology · 2016
    Article
  7. Article
  8. Targeting the Channel Activity of Viroporins.Advances in protein chemistry and structural biology · 2016
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

4 authors at 2 institutions in 1 country.

Laura C EllisDivision of Neurovirology, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America ; Center for Virology and Vaccine Research, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America ; Harvard Program in Virology, Harvard Medical School, Boston, Massachusetts, United States of America.
Elizabeth Norton
Xin Dang
Igor J Koralnik
Beth Israel Deaconess Medical Center · USHarvard University · US

Funding

Role of Inflammation in Progressive Multifocal LeukoencephalopathyR01NS047029 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI KORALNIK, IGOR J. · 2004 to 2018
$6.4M
Pathogenesis of a JC Virus Variant in Pyramidal NeuronsR01NS074995 · NINDS · RUSH UNIVERSITY MEDICAL CENTER · PI KORALNIK, IGOR J. · 2012 to 2016
$1.8M
Translational applications of Progressive Multifocal Leukoencephalopathy studiesK24NS060950 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KORALNIK, IGOR J. · 2008 to 2012
$707k
NINDS NIH HHS K24 NS 060950NINDS NIH HHS K24 NS060950NINDS NIH HHS R01 NS047029NINDS NIH HHS R01 NS 074995NINDS NIH HHS R01 NS074995PHS HHS 047029
6 · The paper itself

Abstract

Infection of glial cells by the human polyomavirus JC (JCV) causes progressive multifocal leukoencephalopathy (PML). JCV Encephalopathy (JCVE) is a newly identified disease characterized by JCV infection of cortical pyramidal neurons. The virus JCVCPN associated with JCVE contains a unique 143 base pair deletion in the agnogene. Contrary to most JCV brain isolates, JCVCPN has an archetype-like regulatory region (RR) usually found in kidney strains. This provided us with the unique opportunity to determine for the first time how each of these regions contributed to the phenotype of JCVCPN. We characterized the replication of JCVCPN compared to the prototype virus JCVMad-1 in kidney, glial and neuronal cell lines. We found that JCVCPN is capable of replicating viral DNA in all cell lines tested, but is unable to establish persistent infection seen with JCVMad-1. JCVCPN does not have an increased ability to replicate in the neuronal cell line tested. To determine whether this phenotype results from the archetype-like RR or the agnogene deletion, we generated chimeric viruses between JCVCPN of JCVMad-1. We found that the deletion in the agnogene is the predominant cause of the inability of the virus to maintain a persistent infection, with the introduction of a full length agnogene, either with or without agnoprotein expression, rescues the replication of JCVCPN. Studying this naturally occurring pathogenic variant of JCV provides a valuable tool for understanding the functions of the agnogene and RR form in JCV replication.

Indexed as

Gene Expression Regulation, ViralVirus AssemblyAnimalsCapsid ProteinsCell LineChlorocebus aethiopsCOS CellsGene DeletionGene OrderHumansJC VirusNeurogliaPhenotypeRecombination, GeneticTranscription, GeneticViral Regulatory and Accessory Proteinsagnoprotein, polyomavirusCapsid ProteinsViral Regulatory and Accessory ProteinsViroporin ProteinsVP1 protein, polyomavirus

Identifiers

PMID24265839
PMCPMC3827225
OpenAlexW2132409729

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.