Evidence map›Paper›PMID 33530371›Full record

ReviewViruses2021

Viral Evasion of RIG-I-Like Receptor-Mediated Immunity through Dysregulation of Ubiquitination and ISGylation.

Cindy Chiang, Guanqun Liu, Michaela U Gack

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  9. Review
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  11. Article
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  14. Article
  15. Review
  16. Article
  17. The Roles of Ubiquitination in Pathogenesis of Influenza Virus Infection.International journal of molecular sciences · 2022
    Review
  18. Review
  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

3 authors at 1 institution in 1 country.

Cindy ChiangFlorida Research and Innovation Center, Cleveland Clinic, Port Saint Lucie, FL 34987, USA.
Guanqun LiuFlorida Research and Innovation Center, Cleveland Clinic, Port Saint Lucie, FL 34987, USA.ORCID 0000-0003-2520-7625
Michaela U GackFlorida Research and Innovation Center, Cleveland Clinic, Port Saint Lucie, FL 34987, USA.
Cleveland Clinic Florida · US

Funding

Regulation of Host Innate Immunity Against Viral InfectionR01AI087846 · NIAID · UNIVERSITY OF CHICAGO · PI GACK, MICHAELA ULRIKE · 2010 to 2020
$3.9M
Regulation of Host Innate Immunity Against Viral InfectionR37AI087846 · NIAID · CLEVELAND CLINIC LERNER COM-CWRU · PI Michaela Ulrike Gack · 2021 to 2026
$2.8M
Flavivirus NS3-mediated Innate Immune EscapeR01AI127774 · NIAID · UNIVERSITY OF CHICAGO · PI GACK, MICHAELA ULRIKE · 2016 to 2020
$2.6M
The Role of TRIM23 in Autophagy Mediated Antiviral DefensesR01AI148534 · NIAID · UNIVERSITY OF CHICAGO · PI GACK, MICHAELA ULRIKE · 2020 to 2024
$2.3M
EBV infection control by RNA surveillanceR21AI148082 · NIAID · UNIVERSITY OF CHICAGO · PI GACK, MICHAELA ULRIKE · 2019 to 2020
$446k
NIAID NIH HHS R01 AI087846NIAID NIH HHS R01 AI127774NIAID NIH HHS R01 AI148534NIAID NIH HHS R21 AI148082NIAID NIH HHS R37 AI087846
6 · The paper itself

Abstract

Viral dysregulation or suppression of innate immune responses is a key determinant of virus-induced pathogenesis. Important sensors for the detection of virus infection are the RIG-I-like receptors (RLRs), which, in turn, are antagonized by many RNA viruses and DNA viruses. Among the different escape strategies are viral mechanisms to dysregulate the post-translational modifications (PTMs) that play pivotal roles in RLR regulation. In this review, we present the current knowledge of immune evasion by viral pathogens that manipulate ubiquitin- or ISG15-dependent mechanisms of RLR activation. Key viral strategies to evade RLR signaling include direct targeting of ubiquitin E3 ligases, active deubiquitination using viral deubiquitinating enzymes (DUBs), and the upregulation of cellular DUBs that regulate RLR signaling. Additionally, we summarize emerging new evidence that shows that enzymes of certain coronaviruses such as SARS-CoV-2, the causative agent of the current COVID-19 pandemic, actively deISGylate key molecules in the RLR pathway to escape type I interferon (IFN)-mediated antiviral responses. Finally, we discuss the possibility of targeting virally-encoded proteins that manipulate ubiquitin- or ISG15-mediated innate immune responses for the development of new antivirals and vaccines.

Indexed as

Immune EvasionCoronavirus 3C ProteasesCytokinesDEAD Box Protein 58HumansImmunity, InnateReceptors, ImmunologicSARS-CoV-2Signal TransductionUbiquitinUbiquitinsVirus DiseasesViruses3C-like proteinase, SARS-CoV-2Coronavirus 3C ProteasesCytokinesDEAD Box Protein 58ISG15 protein, humanReceptors, ImmunologicRIGI protein, humanUbiquitinUbiquitinsinnate immunityinterferonISG15ubiquitinviral evasion

Identifiers

PMID33530371
PMCPMC7910861
OpenAlexW3121226777

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.