Evidence map›Paper›PMID 32852081›Full record

ArticleThe EMBO journal2020

Disrupting HIV-1 capsid formation causes cGAS sensing of viral DNA.

Rebecca P Sumner, Lauren Harrison, Emma Touizer, Thomas P Peacock, Matthew Spencer, Lorena Zuliani-Alvarez, Greg J Towers

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.3field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Unintegrated HIV-1 DNA recruits cGAS via its histone-binding domain to escape innate immunity.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  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

7 authors at 1 institution in 1 country.

Rebecca P SumnerDivision of Infection and Immunity, University College London, London, UK.ORCID 0000-0003-0735-8649
Lauren HarrisonDivision of Infection and Immunity, University College London, London, UK.
Emma TouizerDivision of Infection and Immunity, University College London, London, UK.ORCID 0000-0002-7164-8555
Thomas P PeacockDivision of Infection and Immunity, University College London, London, UK.
Matthew SpencerDivision of Infection and Immunity, University College London, London, UK.
Lorena Zuliani-AlvarezDivision of Infection and Immunity, University College London, London, UK.
Greg J TowersDivision of Infection and Immunity, University College London, London, UK.
University College London · GB

Funding

Medical Research Council G0801172Medical Research Council MR/S023380/1Wellcome TrustWellcome Trust 108183Wellcome Trust 214344
6 · The paper itself

Abstract

Detection of viral DNA by cyclic GMP-AMP synthase (cGAS) is a first line of defence leading to the production of type I interferon (IFN). As HIV-1 replication is not a strong inducer of IFN, we hypothesised that an intact capsid physically cloaks viral DNA from cGAS. To test this, we generated defective viral particles by treatment with HIV-1 protease inhibitors or by genetic manipulation of gag. These viruses had defective Gag cleavage, reduced infectivity and diminished capacity to saturate TRIM5α. Importantly, unlike wild-type HIV-1, infection with cleavage defective HIV-1 triggered an IFN response in THP-1 cells that was dependent on viral DNA and cGAS. An IFN response was also observed in primary human macrophages infected with cleavage defective viruses. Infection in the presence of the capsid destabilising small molecule PF-74 also induced a cGAS-dependent IFN response. These data demonstrate a protective role for capsid and suggest that antiviral activity of capsid- and protease-targeting antivirals may benefit from enhanced innate and adaptive immunity in vivo.

Indexed as

Adaptive ImmunityAntiviral Restriction FactorsCapsidCell LineCRISPR-Cas SystemsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, ViralGene EditingGene Products, gagHIV-1HIV InfectionsHIV Protease InhibitorsHost-Pathogen InteractionsHumansImmunity, InnateIndolesAntiviral Restriction FactorscGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDNA, ViralGene Products, gagHIV Protease InhibitorsIndolesInterferonsMembrane ProteinsNucleotidyltransferasesPF-3450074PhenylalanineSTING1 protein, humanSTING ProteinTRIM5 protein, humanTripartite Motif ProteinsUbiquitin-Protein LigasescapsidcGASDNA sensingHIV-1protease inhibitor

Identifiers

PMID32852081
PMCPMC7560218
OpenAlexW3080577158

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.