Evidence map›Paper›PMID 33652634›Full record

ReviewViruses2021

The Role of the Host Ubiquitin System in Promoting Replication of Emergent Viruses.

Karl M Valerdi, Adam Hage, Sarah van Tol, Ricardo Rajsbaum, Maria I Giraldo

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 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. 25 Years of Ebola Virus VP35 Research.Journal of molecular biology · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Impaired K48-polyubiquitination downmodulates mouse norovirus propagation.Frontiers in cellular and infection microbiology · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

5 authors at 1 institution in 1 country.

Karl M ValerdiDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0002-7160-2602
Adam HageDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0001-7668-892X
Sarah van TolDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Ricardo RajsbaumDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0002-5058-5444
Maria I GiraldoDepartment of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA.
The University of Texas Medical Branch at Galveston · US

Funding

UTMB WOMEN'S HEALTH RESEARCH SCHOLARS PROGRAMK12HD052023 · NICHD · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BERENSON, ABBEY B · 2005 to 2023
$8.1M
Regulation of Ebola virus replication by the host ubiquitin systemR01AI134907 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GIRALDO, MARIA ISABEL · 2018 to 2022
$3.1M
EMERGING AND TROPICAL INFECTIOUS DISEASEST32AI007526 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SOONG, LYNN · 1997 to 2025
$3.1M
Biodefense Training ProgramT32AI060549 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ASHOK K CHOPRA, Janice J Endsley · 2004 to 2026
$3.0M
PREPing for SUCCESSR25GM134990 · NIGMS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI VARGAS, GRACIE · 2020 to 2024
$1.2M
NIAID NIH HHS R01 AI134907NIAID NIH HHS T32 AI007526NIAID NIH HHS T32 AI060549NIGMS NIH HHS R25 GM134990
6 · The paper itself

Abstract

Ubiquitination of proteins is a post-translational modification process with many different cellular functions, including protein stability, immune signaling, antiviral functions and virus replication. While ubiquitination of viral proteins can be used by the host as a defense mechanism by destroying the incoming pathogen, viruses have adapted to take advantage of this cellular process. The ubiquitin system can be hijacked by viruses to enhance various steps of the replication cycle and increase pathogenesis. Emerging viruses, including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), flaviviruses like Zika and dengue, as well as highly pathogenic viruses like Ebola and Nipah, have the ability to directly use the ubiquitination process to enhance their viral-replication cycle, and evade immune responses. Some of these mechanisms are conserved among different virus families, especially early during virus entry, providing an opportunity to develop broad-spectrum antivirals. Here, we discuss the mechanisms used by emergent viruses to exploit the host ubiquitin system, with the main focus on the role of ubiquitin in enhancing virus replication.

Indexed as

Virus ReplicationImmune EvasionUbiquitinUbiquitinationViral ProteinsVirus AssemblyVirus DiseasesVirusesVirus InternalizationVirus ReleaseUbiquitinViral Proteinsantagonism of immune responseEbolaemergent virusesNipahpro-viral functionSARS-CoV-2tripartite motif (TRIM) proteinsubiquitin systemZika

Identifiers

PMID33652634
PMCPMC7996891
OpenAlexW3134179058

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.