Evidence map›Paper›PMID 28576494›Full record

ReviewBiochemical and biophysical research communications2017

Antagonism of type I interferon by flaviviruses.

Lisa Miorin, Ana M Maestre, Ana Fernandez-Sesma, Adolfo García-Sastre

Abstract readReview
In one paragraph

Review in Biochemical and biophysical research communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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

64 citing papers in PubMed.

  1. Powassan Virus NS5 Antagonizes TYK2-Mediated Immune Signaling Pathways.bioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Review
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  5. Article
  6. Review
  7. Article
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  9. Innate Immune and Inflammatory Responses to Dengue Virus Infection.Current topics in microbiology and immunology · 2026
    Review
  10. Cellular Biology: Virus-Host Interactions and RNA Structure and Function.Current topics in microbiology and immunology · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

4 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

4 authors.

Lisa MiorinDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
Ana M MaestreDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States.
Ana Fernandez-SesmaDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States. Electronic address: ana.sesma@mssm.edu.
Adolfo García-SastreDepartment of Microbiology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Global Health and Emerging Pathogens Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States; Department of Medicine, Division of Infectious Diseases, Icahn School of Medicine at Mount Sinai, New York, NY 10029, United States. Electronic address: Adolfo.Garcia-Sastre@mssm.edu.

Funding

Project 3 - Ex vivo immune profiling of dengue viruses and vaccinesU19AI118610 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI MERAD, MIRIAM · 2015 to 2021
$46.6M
MODULATION OF INNATE AND ADAPTIVE IMMUNITY BY DENGUE VIRUSR01AI073450 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FERNANDEZ-SESMA, ANA · 2008 to 2017
$3.3M
HUMAN TONSIL EXPLANTS AS A NOVEL MODEL FOR STUDYING DENGUE VIRUS INFECTIONR21AI116022 · NIAID · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI FERNANDEZ-SESMA, ANA · 2015 to 2016
$461k
NIAID NIH HHS R01 AI073450NIAID NIH HHS R21 AI116022NIAID NIH HHS U19 AI118610
6 · The paper itself

Abstract

The prompt and tightly controlled induction of type I interferon is a central event of the immune defense against viral infection. Flaviviruses comprise a large family of arthropod-borne positive-stranded RNA viruses, many of which represent a serious threat to global human health due to their high rates of morbidity and mortality. All flaviviruses studied so far have been shown to counteract the host's immune response to establish a productive infection and facilitate viral spread. Here, we review the current knowledge on the main strategies that human pathogenic flaviviruses utilize to escape both type I IFN induction and effector pathways. A better understanding of the specific mechanisms by which flaviviruses activate and evade innate immune responses is critical for the development of better therapeutics and vaccines.

Indexed as

AnimalsFlavivirusFlavivirus InfectionsHost-Pathogen InteractionsHumansImmunity, InnateInterferon Type IModels, ImmunologicalVirus ReplicationInterferon Type IFlavivirusesInnate immunityInterferon antagonismType I interferonViral innate immune evasion

Identifiers

PMID28576494
PMCPMC5626595

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.