Evidence map›Paper›PMID 24158625›Full record

ArticleGenome biology and evolution2013

An evolutionary screen highlights canonical and noncanonical candidate antiviral genes within the primate TRIM gene family.

Ray Malfavon-Borja, Sara L Sawyer, Lily I Wu, Michael Emerman, Harmit S Malik

Open access · goldAbstract read
In one paragraph

Article in Genome biology and evolution, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 28% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Interplay between TRIM7 and antiviral immunity.Frontiers in cellular and infection microbiology · 2023
    Review
  9. Trim69 is a microtubule regulator that acts as a pantropic viral inhibitor.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  10. Article
  11. Article
  12. CoelacanthJournal of virology · 2021
    Article
  13. Article
  14. Article
  15. 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 3 institutions in 1 country.

Ray Malfavon-BorjaDepartment of Genome Sciences, University of Washington.
Sara L Sawyer
Lily I Wu
Michael Emerman
Harmit S Malik
Fred Hutch Cancer Center · USThe University of Texas at Austin · USUniversity of Washington · US

Funding

Interdisciplinary Tranining in Cancer ResearchT32CA080416 · NCI · UNIVERSITY OF WASHINGTON · PI STODDARD, BARRY L. · 1998 to 2023
$9.7M
VPR AND HIV INFECTIONR01AI030927 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EMERMAN, MICHAEL · 1991 to 2020
$5.3M
VPR AND HIV INFECTIONR37AI030927 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI EMERMAN, MICHAEL · 2001 to 2010
$4.6M
Howard Hughes Medical InstituteNCI NIH HHS T32 CA080416NCI NIH HHS T32 CA80416NIAID NIH HHS R01 AI030927NIAID NIH HHS R37 AI030927NIAID NIH HHS R37 AI30927PHS HHS F31 A1084620
6 · The paper itself

Abstract

Recurrent viral pressure has acted on host-encoded antiviral genes during primate and mammalian evolution. This selective pressure has resulted in dramatic episodes of adaptation in host antiviral genes, often detected via positive selection. These evolutionary signatures of adaptation have the potential to highlight previously unrecognized antiviral genes (also called restriction factors). Although the TRIM multigene family is recognized for encoding several bona fide restriction factors (e.g., TRIM5alpha), most members of this expansive gene family remain uncharacterized. Here, we investigated the TRIM multigene family for signatures of positive selection to identify novel candidate antiviral genes. Our analysis reveals previously undocumented signatures of positive selection in 17 TRIM genes, 10 of which represent novel candidate restriction factors. These include the unusual TRIM52 gene, which has evolved under strong positive selection despite its encoded protein lacking a putative viral recognition (B30.2) domain. We show that TRIM52 arose via gene duplication from the TRIM41 gene. Both TRIM52 and TRIM41 have dramatically expanded RING domains compared with the rest of the TRIM multigene family, yet this domain has evolved under positive selection only in primate TRIM52, suggesting that it represents a novel host-virus interaction interface. Our evolutionary-based screen not only documents positive selection in known TRIM restriction factors but also highlights candidate novel restriction factors, providing insight into the interfaces of host-pathogen interactions mediated by the TRIM multigene family.

Indexed as

Evolution, MolecularMultigene FamilyAmino Acid SequenceAnimalsCarrier ProteinsHost-Pathogen InteractionsHumansMolecular Sequence DataNuclear ProteinsPrimatesProtein BindingRING Finger DomainsSelection, GeneticUbiquitin-Protein LigasesCarrier ProteinsNuclear ProteinsTRIM41 protein, humanUbiquitin-Protein LigasesdN/dSpositive selectionrestriction factorsTRIM5TRIM52

Identifiers

PMID24158625
PMCPMC3845644
OpenAlexW2150313578

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LicenceCC BY-NC
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Registered trials

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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.