Evidence map›Paper›PMID 31251739›Full record

ArticlePLoS neglected tropical diseases2019

The E3 ligase TRIM56 is a host restriction factor of Zika virus and depends on its RNA-binding activity but not miRNA regulation, for antiviral function.

Darong Yang, Nan L Li, Dahai Wei, Baoming Liu, Fang Guo, Husni Elbahesh, Yunzhi Zhang, Zhi Zhou, Guo-Yun Chen, Kui Li

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. The regulation of innate antiviral immunity by TRIM56.Infectious diseases & immunity · 2025
    Review
  7. Review
  8. Review
  9. The Magic and Mystery of TRIM65 in Diseases.Current medicinal chemistry · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Viruses · 2024
    Article
  19. Article
  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

10 authors at 3 institutions in 2 countries.

Darong YangDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Nan L LiDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Dahai WeiDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Baoming LiuDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.ORCID 0000-0003-2204-9828
Fang GuoBaruch S. Blumberg Institute, Doylestown, PA, United States of America.
Husni ElbaheshDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Yunzhi ZhangDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Zhi ZhouDepartment of Infectious Diseases, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Guo-Yun ChenChildren's Foundation Research Institute at Le Bonheur Children's Hospital, Department of Pediatrics, University of Tennessee Health Science Center, Memphis, TN, United States of America.
Kui LiDepartment of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, United States of America.ORCID 0000-0002-2413-6020
University of Tennessee Health Science Center · USBaruch S. Blumberg Institute · USDalian Medical University · CN

Funding

Role of TLR3 Signaling in Control of HCVR01AI069285 · NIAID · UNIVERSITY OF TEXAS MED BR GALVESTON · PI LI, KUI · 2007 to 2016
$2.5M
Targeting Siglec-9/E for therapy of sepsisR01AI137255 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CHEN, GUOYUN · 2018 to 2022
$1.9M
TRIMing Flavivirus Infection by a Host-encoded E3 LigaseR21AI137812 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, KUI · 2018 to 2019
$418k
Role of TLR3 Signaling in Control of HCVR56AI069285 · NIAID · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI LI, KUI · 2012 to 2012
$300k
NIAID NIH HHS R01 AI069285NIAID NIH HHS R01 AI137255NIAID NIH HHS R21 AI137812NIAID NIH HHS R56 AI069285
6 · The paper itself

Abstract

Infection by Zika virus (ZIKV) is linked to microcephaly and other neurological disorders, posing a significant health threat. Innate immunity is the first line of defense against invading pathogens, but relatively little is understood regarding host intrinsic mechanisms that guard against ZIKV. Here, we show that host tripartite motif-containing protein 56 (TRIM56) poses a barrier to ZIKV infection in cells of neural, epithelial and fibroblast origins. Overexpression of TRIM56, but not an E3 ligase-dead mutant or one lacking a short C-terminal portion, inhibited ZIKV RNA replication. Conversely, depletion of TRIM56 increased viral RNA levels. Although the C-terminal region of TRIM56 bears sequence homology to NHL repeat of TRIM-NHL proteins that regulate miRNA activity, knockout of Dicer, which abolishes production of miRNAs, had no demonstrable effect on ZIKV restriction imposed by TRIM56. Rather, we found that TRIM56 is an RNA-binding protein that associates with ZIKV RNA in infected cells. Moreover, a recombinant TRIM56 fragment comprising the C-terminal 392 residues captured ZIKV RNA in cell-free reactions, indicative of direct interaction. Remarkably, deletion of a short C-terminal tail portion abrogated the TRIM56-ZIKV RNA interaction, concomitant with a loss in antiviral activity. Altogether, our study reveals TRIM56 is an RNA binding protein that acts as a ZIKV restriction factor and provides new insights into the antiviral mechanism by which this E3 ligase tackles flavivirus infections.

Indexed as

Epithelial CellsFibroblastsHumansImmunologic FactorsMicroRNAsNeuronsProtein BindingRNA-Binding ProteinsRNA, ViralTripartite Motif ProteinsUbiquitin-Protein LigasesVirus ReplicationZika VirusImmunologic FactorsMicroRNAsRNA-Binding ProteinsRNA, ViralTRIM56 protein, humanTripartite Motif ProteinsUbiquitin-Protein Ligases

Identifiers

PMID31251739
PMCPMC6623546
OpenAlexW2954747355

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.