Evidence map›Paper›PMID 21079688›Full record

ArticlePLoS pathogens2010

HTLV-1 evades type I interferon antiviral signaling by inducing the suppressor of cytokine signaling 1 (SOCS1).

Stéphanie Olière, Eduardo Hernandez, Agnès Lézin, Meztli Arguello, Renée Douville, Thi Lien-Anh Nguyen, Stéphane Olindo, Gérard Panelatti, Mirdad Kazanji, Peter Wilkinson and 3 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PLoS pathogens, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  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

13 authors at 5 institutions in 3 countries.

Stéphanie OlièreMolecular Oncology Group, Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada.
Eduardo Hernandez
Agnès Lézin
Meztli Arguello
Renée Douville
Thi Lien-Anh Nguyen
Stéphane Olindo
Gérard Panelatti
Mirdad Kazanji
Peter Wilkinson
Rafick-Pierre Sékaly
Raymond Césaire
John Hiscott
Centre Hospitalier Universitaire de Martinique · MQJewish General Hospital · CAMcGill University · CACentre Hospitalier de l’Université de Montréal · CACentre International de Recherches Médicales de Franceville · GA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent of Adult T cell Leukemia (ATL) and the neurological disorder HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Although the majority of HTLV-1-infected individuals remain asymptomatic carriers (AC) during their lifetime, 2-5% will develop either ATL or HAM/TSP, but never both. To better understand the gene expression changes in HTLV-1-associated diseases, we examined the mRNA profiles of CD4+ T cells isolated from 7 ATL, 12 HAM/TSP, 11 AC and 8 non-infected controls. Using genomic approaches followed by bioinformatic analysis, we identified gene expression pattern characteristic of HTLV-1 infected individuals and particular disease states. Of particular interest, the suppressor of cytokine signaling 1--SOCS1--was upregulated in HAM/TSP and AC patients but not in ATL. Moreover, SOCS1 was positively correlated with the expression of HTLV-1 mRNA in HAM/TSP patient samples. In primary PBMCs transfected with a HTLV-1 proviral clone and in HTLV-1-transformed MT-2 cells, HTLV-1 replication correlated with induction of SOCS1 and inhibition of IFN-α/β and IFN-stimulated gene expression. Targeting SOCS1 with siRNA restored type I IFN production and reduced HTLV-1 replication in MT-2 cells. Conversely, exogenous expression of SOCS1 resulted in enhanced HTLV-1 mRNA synthesis. In addition to inhibiting signaling downstream of the IFN receptor, SOCS1 inhibited IFN-β production by targeting IRF3 for ubiquitination and proteasomal degradation. These observations identify a novel SOCS1 driven mechanism of evasion of the type I IFN antiviral response against HTLV-1.

Indexed as

AdultAntiviral AgentsBiomarkers, TumorBlotting, WesternCase-Control StudiesCD4-Positive T-LymphocytesCells, CulturedGene Expression ProfilingHTLV-I InfectionsHumansHuman T-lymphotropic virus 1ImmunoblottingImmunoprecipitationInterferon Type IOligonucleotide Array Sequence AnalysisParaparesis, Tropical SpasticAntiviral AgentsBiomarkers, TumorInterferon Type IRNA, MessengerRNA, Small InterferingRNA, ViralSOCS1 protein, humanSuppressor of Cytokine Signaling 1 ProteinSuppressor of Cytokine Signaling Proteins

Identifiers

PMID21079688
PMCPMC2973829
OpenAlexW2057844985

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.