Evidence map›Paper›PMID 33362792›Full record

ReviewFrontiers in immunology2020

All About the RNA: Interferon-Stimulated Genes That Interfere With Viral RNA Processes.

Emily Yang, Melody M H Li

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed, 2 pooled it
6.4field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 2 syntheses or guidelines pooled it, 162 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Viruses in bronchiectasis.ERJ open research · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Central TYK2 inhibition identifies TYK2 as a key neuroimmune modulator.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article

39 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

2 authors at 1 institution in 1 country.

Emily YangMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, United States.
Melody M H LiMolecular Biology Institute, University of California, Los Angeles, Los Angeles, CA, United States.
University of California, Los Angeles · US

Funding

MULTIDISCIPLINARY TRAINING IN MICROBIAL PATHOGENESIST32AI007323 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Peter John Bradley · 1988 to 2026
$8.6M
NIAID NIH HHS T32 AI007323
6 · The paper itself

Abstract

Interferon (IFN) signaling induces the expression of a wide array of genes, collectively referred to as IFN-stimulated genes (ISGs) that generally function to inhibit viral replication. RNA viruses are frequently targeted by ISGs through recognition of viral replicative intermediates and molecular features associated with viral genomes, or the lack of molecular features associated with host mRNAs. The ISGs reviewed here primarily inhibit viral replication in an RNA-centric manner, working to sense, degrade, or repress expression of viral RNA. This review focuses on dissecting how these ISGs exhibit multiple antiviral mechanisms, often through use of varied co-factors, highlighting the complexity of the type I IFN response. Specifically, these ISGs can mediate antiviral effects through viral RNA degradation, viral translation inhibition, or both. While the OAS/RNase L pathway globally degrades RNA and arrests translation, ISG20 and ZAP employ targeted RNA degradation and translation inhibition to block viral replication. Meanwhile, SHFL targets translation by inhibiting -1 ribosomal frameshifting, which is required by many RNA viruses. Finally, a number of E3 ligases inhibit viral transcription, an attractive antiviral target during the lifecycle of negative-sense RNA viruses which must transcribe their genome prior to translation. Through this review, we aim to provide an updated perspective on how these ISGs work together to form a complex network of antiviral arsenals targeting viral RNA processes.

Indexed as

RNA Processing, Post-TranscriptionalVirus Replication2',5'-Oligoadenylate SynthetaseAnimalsEndoribonucleasesGene Expression Regulation, ViralHost-Pathogen InteractionsHumansInterferon Regulatory FactorsRNA StabilityRNA, ViralTranscription, GeneticUbiquitinationUbiquitin-Protein LigasesVirus DiseasesViruses2-5A-dependent ribonuclease2',5'-Oligoadenylate SynthetaseEndoribonucleasesInterferon Regulatory FactorsRNA, ViralUbiquitin-Protein Ligasesco-factorsinterferon-stimulated genesRNA sensingtranslation inhibitionviral RNA degradation

Identifiers

PMID33362792
PMCPMC7756014
OpenAlexW3111912998

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.