Evidence map›Paper›PMID 34578420›Full record

ReviewViruses2021

Type I Interferon Induction and Exhaustion during Viral Infection: Plasmacytoid Dendritic Cells and Emerging COVID-19 Findings.

Trever T Greene, Elina I Zuniga

Open access · goldAbstract readReview
In one paragraph

Review in Viruses, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.4field-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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Innate immunity to SARS-CoV-2 infection: a review.Epidemiology and infection · 2022
    Pooled it
  2. Article
  3. Immune cell disorder in viral pneumonia.Journal of translational medicine · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Antiviral Therapy of COVID-19.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Review
  19. Emerging Effects of IL-33 on COVID-19.International journal of molecular sciences · 2022
    Review
  20. COVID-19 and Gut Injury.Nutrients · 2022
    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 1 institution in 1 country.

Trever T GreeneDivision of Biological Sciences, University of California, San Diego, CA 92093, USA.
Elina I ZunigaDivision of Biological Sciences, University of California, San Diego, CA 92093, USA.
University of California, San Diego · US

Funding

UC San Diego Clinical and Translational Research InstituteUL1TR001442 · NCATS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FIRESTEIN, GARY S, HOGARTH, MICHAEL · 2015 to 2024
$88.3M
VirologyP30AI036214 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI David Mitchell Smith · 1994 to 2026
$78.4M
Single-Cell Transcriptomic and Epigenetics CoreP01AI132122 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GOLDRATH, ANANDA W · 2018 to 2022
$9.8M
NCATS NIH HHS UL1 TR001442NIAID NIH HHS P01 AI132122NIAID NIH HHS P30 AI036214NIH HHS AI081923NIH HHS AI113923NIH HHS AI132122NIH HHS AI145314
6 · The paper itself

Abstract

Type I Interferons (IFN-I) are a family of potent antiviral cytokines that act through the direct restriction of viral replication and by enhancing antiviral immunity. However, these powerful cytokines are a caged lion, as excessive and sustained IFN-I production can drive immunopathology during infection, and aberrant IFN-I production is a feature of several types of autoimmunity. As specialized producers of IFN-I plasmacytoid (p), dendritic cells (DCs) can secrete superb quantities and a wide breadth of IFN-I isoforms immediately after infection or stimulation, and are the focus of this review. Notably, a few days after viral infection pDCs tune down their capacity for IFN-I production, producing less cytokines in response to both the ongoing infection and unrelated secondary stimulations. This process, hereby referred to as "pDC exhaustion", favors viral persistence and associates with reduced innate responses and increased susceptibility to secondary opportunistic infections. On the other hand, pDC exhaustion may be a compromise to avoid IFN-I driven immunopathology. In this review we reflect on the mechanisms that initially induce IFN-I and subsequently silence their production by pDCs during a viral infection. While these processes have been long studied across numerous viral infection models, the 2019 coronavirus disease (COVID-19) pandemic has brought their discussion back to the fore, and so we also discuss emerging results related to pDC-IFN-I production in the context of COVID-19.

Indexed as

Host-Pathogen InteractionsBiomarkersCOVID-19CytokinesDendritic CellsHumansImmunity, InnateImmunomodulationInterferon Type ISARS-CoV-2Toll-Like ReceptorsBiomarkersCytokinesInterferon Type IToll-Like ReceptorsCOVID-19HBVHCVHIV-1IFN-IinfluenzaLCMVplasmacytoid dendritic cellsSARS-CoV-2viral infection

Identifiers

PMID34578420
PMCPMC8472174
OpenAlexW3200571768

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.