Evidence map›Paper›PMID 30132758›Full record

ArticleeLife2018

The aryl hydrocarbon receptor and interferon gamma generate antiviral states via transcriptional repression.

Tonya Kueck, Elena Cassella, Jessica Holler, Baek Kim, Paul D Bieniasz

Open access · goldAbstract read
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
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  5. Review
  6. Article
  7. The role of the AHR in host-pathogen interactions.Nature reviews. Immunology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. When AHR signaling pathways meet viral infections.Cell communication and signaling : CCS · 2023
    Review
  16. Article
  17. Review
  18. Article
  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

5 authors at 3 institutions in 2 countries.

Tonya KueckLaboratory of Retrovirology, The Rockefeller University, New York, United States.
Elena CassellaLaboratory of Retrovirology, The Rockefeller University, New York, United States.
Jessica HollerCenter for Drug Discovery, The Department of Pediatrics, Emory University, Atlanta, United States.
Baek KimCenter for Drug Discovery, The Department of Pediatrics, Emory University, Atlanta, United States.
Paul D BieniaszLaboratory of Retrovirology, The Rockefeller University, New York, United States.ORCID http://orcid.org/0000-0002-2368-3719
Emory University · USRockefeller University · USHoward Hughes Medical Institute · US

Funding

Discovery and Mechanism of Antiretroviral FactorsR37AI064003 · NIAID · ROCKEFELLER UNIVERSITY · PI BIENIASZ, PAUL D. · 2011 to 2020
$4.9M
Lentivirus Replication Strategy and PathogenesisR01AI136581 · NIAID · EMORY UNIVERSITY · PI Baek Kim · 2018 to 2026
$3.9M
SAMHD1 controls dNTP pool and HIV sensitivity to NRTIsR01GM104198 · NIGMS · UNIVERSITY OF ROCHESTER · PI KIM, BAEK · 2012 to 2018
$2.3M
Howard Hughes Medical InstituteNational Institute of Allergy and Infectious Diseases R01 AI136581National Institute of Allergy and Infectious Diseases R37AI64003NIAID NIH HHS R01 AI136581NIAID NIH HHS R37 AI064003NIGMS NIH HHS R01 GM104198
6 · The paper itself

Abstract

The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor whose activation induces the expression of numerous genes, with many effects on cells. However, AhR activation is not known to affect the replication of viruses. We show that AhR activation in macrophages causes a block to HIV-1 and HSV-1 replication. We find that AhR activation transcriptionally represses cyclin-dependent kinase (CDK)1/2 and their associated cyclins, thereby reducing SAMHD1 phosphorylation, cellular dNTP levels and both HIV-1 and HSV-1 replication. Remarkably, a different antiviral stimulus, interferon gamma (IFN-γ), that induces a largely non-overlapping set of genes, also transcriptionally represses CDK1, CDK2 and their associated cyclins, resulting in similar dNTP depletion and antiviral effects. Concordantly, the SIV Vpx protein provides complete and partial resistance to the antiviral effects of AhR and IFN-γ, respectively. Thus, distinct antiviral signaling pathways converge on CDK/cyclin repression, causing inhibition of viral DNA synthesis and replication.

Indexed as

Transcription, GeneticAnimalsAntiviral AgentsCell CycleCell Line, TumorCyclin-Dependent KinasesCyclinsGene Expression RegulationHIV-1HumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaMacrophage ActivationMacrophagesModels, BiologicalNucleotidesAntiviral AgentsCyclin-Dependent KinasesCyclinsIDO1 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaNucleotidesReceptors, Aryl HydrocarbonRNA, MessengerSAM Domain and HD Domain-Containing Protein 1STAT1 Transcription FactorViral Regulatory and Accessory ProteinsVPX protein, Simian immunodeficiency virusaryl hydrocarbon receptorHIV-1HSVhumanimmunologyinfectious diseaseinflammationInterferon-gammamicrobiologySAMDH1virus

Identifiers

PMID30132758
PMCPMC6120754
OpenAlexW2951573264

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.