Evidence map›Paper›PMID 25771184›Full record

ReviewCurrent opinion in immunology2015

New insights into type I interferon and the immunopathogenesis of persistent viral infections.

Laura M Snell, David G Brooks

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. The balance between gasdermin D and STING signaling shapes the severity of schistosome immunopathology.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Tumor-Specific CD4Frontiers in immunology · 2022
    Article
  11. Review
  12. Article
  13. Chronic virus infection drives CD8 T cell-mediated thymic destruction and impaired negative selection.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Trisomy 21 dysregulates T cell lineages toward an autoimmunity-prone state associated with interferon hyperactivity.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  18. Article
  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

2 authors at 2 institutions in 2 countries.

Laura M SnellDepartment of Microbiology, Immunology and Molecular Genetics and UCLA AIDS Institute, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, United States.
David G BrooksDepartment of Microbiology, Immunology and Molecular Genetics and UCLA AIDS Institute, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, United States; Princess Margaret Cancer Center, University Health Network and the Department of Immunology, University of Toronto, Toronto, Ontario, M5G 2M9 Canada. Electronic address: dbrooks@microbio.ucla.edu.
Black AIDS Institute · USUniversity of California, Los Angeles · US

Funding

Mechanisms of Viral PersistenceR01AI085043 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2010 to 2023
$4.5M
Immune Regulation of Viral Persistence and Clearance U01AI082975 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2009 to 2013
$2.0M
Restoring antibody effector function during persistent virus infectionR21AI109627 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BROOKS, DAVID G · 2014 to 2015
$358k
NIAID NIH HHS AI082975NIAID NIH HHS AI109627NIAID NIH HHS R01 AI085043NIAID NIH HHS R21 AI109627NIAID NIH HHS U01 AI082975PHS HHS I085043
6 · The paper itself

Abstract

Most viruses generate potent T cell responses that rapidly control infection. However, certain viruses can subvert the immune response to establish persistent infections. The inability to clear virus induces an immunosuppressive program leading to the sustained expression of many immunoregulatory molecules that down-regulate T cell responses. Further, viral persistence is associated with multiple immune dysfunctions including lymphoid disorganization, defective antigen presentation, aberrant B cell responses and hypergammaglobulinemia. Although best known for its antiviral activity, recent data has highlighted the role of type I IFN (IFN-I) signaling as a central mediator of immunosuppression during viral persistence. It is also becoming increasingly apparent that many of the immune dysfunctions during persistent virus infection can be attributed directly or indirectly to the effects of chronic IFN-I signaling. This review explores the increasingly complex role of IFN-I in the regulation of immunity against persistently replicating virus infections and examines current and potential uses of IFN-I and blockade of IFN-I signaling to dampen chronic inflammation and activation in the clinic.

Indexed as

AnimalsChronic DiseaseDendritic CellsHumansInterferon Type ISignal TransductionT-LymphocytesVirus DiseasesInterferon Type I

Identifiers

PMID25771184
PMCPMC4444376
OpenAlexW2017634591

What OpenQuestion holds

Textmetadata
LicenceTDM
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.