Evidence map›Paper›PMID 21543483›Full record

ArticleJournal of virology2011

Beta interferon controls West Nile virus infection and pathogenesis in mice.

Helen M Lazear, Amelia K Pinto, Matthew R Vogt, Michael Gale, Michael S Diamond

Abstract read
In one paragraph

Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
11.3field-weighted citation impact, top 1% 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

75 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
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  8. MITD1 is a brain-specific interferon-inducible factor that inhibits flavivirus replication.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. UFMylation promotes orthoflavivirus infectious particle production.bioRxiv : the preprint server for biology · 2025
    Article
  10. Review
  11. Ocular Manifestations of Flavivirus Infections.Pathogens (Basel, Switzerland) · 2023
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

15 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Helen M LazearDepartment of Medicine, Washington University School of Medicine, 660 South Euclid Avenue, Box 8051, St. Louis, MO 63110, USA.
Amelia K Pinto
Matthew R Vogt
Michael Gale
Michael S Diamond
Washington University in St. Louis · USUniversity of Washington · US

Funding

The Burden of Chikungunya and Dengue Infection in KenyaU54AI081680 · NIAID · OREGON HEALTH & SCIENCE UNIVERSITY · PI RYMAN, KATHERINE D · 2009 to 2013
$40.4M
West Nile Virus and host control of innate defensesU19AI083019 · NIAID · UNIVERSITY OF WASHINGTON · PI CLARK, EDWARD A · 2009 to 2018
$22.5M
Infectious Diseases/Basic Microbial Pathogenic MechanismsT32AI007172 · NIAID · WASHINGTON UNIVERSITY · PI Daniel E. Goldberg, JENNIFER A PHILIPS · 1985 to 2026
$13.0M
Cell-Specific Programs of Host Defense Against West Nile VirusR01AI074973 · NIAID · UNIVERSITY OF WASHINGTON · PI GALE, MICHAEL · 2009 to 2010
$774k
NIAID NIH HHS R01 AI074973NIAID NIH HHS T32 AI007172NIAID NIH HHS T32-AI007172NIAID NIH HHS U19 AI083019NIAID NIH HHS U54 AI081680
6 · The paper itself

Abstract

Studies with mice lacking the common plasma membrane receptor for type I interferon (IFN-αβR(-)(/)(-)) have revealed that IFN signaling restricts tropism, dissemination, and lethality after infection with West Nile virus (WNV) or several other pathogenic viruses. However, the specific functions of individual IFN subtypes remain uncertain. Here, using IFN-β(-)(/)(-) mice, we defined the antiviral and immunomodulatory function of this IFN subtype in restricting viral infection. IFN-β(-)(/)(-) mice were more vulnerable to WNV infection than wild-type mice, succumbing more quickly and with greater overall mortality, although the phenotype was less severe than that of IFN-αβR(-)(/)(-) mice. The increased susceptibility of IFN-β(-)(/)(-) mice was accompanied by enhanced viral replication in different tissues. Consistent with a direct role for IFN-β in control of WNV replication, viral titers in ex vivo cultures of macrophages, dendritic cells, fibroblasts, and cerebellar granule cell neurons, but not cortical neurons, from IFN-β(-)(/)(-) mice were greater than in wild-type cells. Although detailed immunological analysis revealed no major deficits in the quality or quantity of WNV-specific antibodies or CD8(+) T cells, we observed an altered CD4(+) CD25(+) FoxP3(+) regulatory T cell response, with greater numbers after infection. Collectively, these results suggest that IFN-β controls WNV pathogenesis by restricting infection in key cell types and by modulating T cell regulatory networks.

Indexed as

AnimalsInterferon-betaMiceMice, Inbred C57BLMice, KnockoutT-LymphocytesWest Nile FeverInterferon-beta

Identifiers

PMID21543483
PMCPMC3126609
OpenAlexW2117415703

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.