Evidence map›Paper›PMID 34835115›Full record

ReviewViruses2021

How Influenza A Virus NS1 Deals with the Ubiquitin System to Evade Innate Immunity.

Laurie-Anne Lamotte, Lionel Tafforeau

Abstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. TRIM21 is a molecular rheostat for influenza A virus replication.bioRxiv : the preprint server for biology · 2026
    Article
  2. The strategies and advances of mRNA translation booster.Asian journal of pharmaceutical sciences · 2025
    Review
  3. Bacterial Puppeteering: How the Stealth BacteriumPathogens (Basel, Switzerland) · 2025
    Review
  4. Article
  5. Review
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  7. Article
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  12. Article
  13. Article
  14. Article
  15. The Key Role of Lysosomal Protease Cathepsins in Viral Infections.International journal of molecular sciences · 2022
    Review
  16. The Roles of Ubiquitination in Pathogenesis of Influenza Virus Infection.International journal of molecular sciences · 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.

Laurie-Anne LamotteCell Biology Laboratory, Research Institute for Biosciences, Research Institute for Health Sciences and Technology, University of Mons, 7000 Mons, Belgium.ORCID 0000-0002-6691-7570
Lionel TafforeauCell Biology Laboratory, Research Institute for Biosciences, Research Institute for Health Sciences and Technology, University of Mons, 7000 Mons, Belgium.ORCID 0000-0002-8468-7422

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitination is a post-translational modification regulating critical cellular processes such as protein degradation, trafficking and signaling pathways, including activation of the innate immune response. Therefore, viruses, and particularly influenza A virus (IAV), have evolved different mechanisms to counteract this system to perform proper infection. Among IAV proteins, the non-structural protein NS1 is shown to be one of the main virulence factors involved in these viral hijackings. NS1 is notably able to inhibit the host's antiviral response through the perturbation of ubiquitination in different ways, as discussed in this review.

Indexed as

Influenza, HumanOrthomyxoviridae InfectionsAnimalsHumansImmunity, InnateInfluenza A virusUbiquitinViral Nonstructural ProteinsINS1 protein, influenza virusUbiquitinViral Nonstructural Proteinscytokinesinfluenza A virusinnate immunityinterferonISGNEDD8NS1RIG-ISUMOTRIM25ubiquitin

Identifiers

PMID34835115
PMCPMC8619935

What Socratic 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 Socratic graph.