Evidence map›Paper›PMID 29793952›Full record

ArticleJournal of virology2018

Herpes Simplex Virus 1 Tegument Protein VP22 Abrogates cGAS/STING-Mediated Antiviral Innate Immunity.

Jian Huang, Hongjuan You, Chenhe Su, Yangxin Li, Shunhua Chen, Chunfu Zheng

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
7.8field-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

133 citing papers in PubMed, 185 citations in OpenAlex.

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  15. Unraveling the complexities of neurotropic virus infection and immune evasion.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Alternative cGAS signaling promotes herpes simplex encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Review

73 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 5 institutions in 3 countries.

Jian HuangSoochow University, Institutes of Biology and Medical Sciences, Suzhou, China.
Hongjuan YouSoochow University, Institutes of Biology and Medical Sciences, Suzhou, China.
Chenhe SuLady Davis Institute-Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
Yangxin LiInstitute for Cardiovascular Science and Department of Cardiovascular Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Shunhua ChenMicrobiology and Immunology College of Medicine, National Cheng Kung University, Tainan, Taiwan, Republic of China.ORCID 0000-0002-4585-9279
Chunfu ZhengDepartment of Microbiology, Immunology and Infectious Diseases, University of Calgary, Calgary, Alberta, Canada.ORCID 0000-0002-8797-1322
Soochow University · CNFujian Medical University · CNJewish General Hospital · CANational Cheng Kung University · TWXuzhou Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytosolic DNA arising from intracellular pathogens is sensed by cyclic GMP-AMP synthase (cGAS) and triggers a powerful innate immune response. However, herpes simplex virus 1 (HSV-1), a double-stranded DNA virus, has developed multiple mechanisms to attenuate host antiviral machinery and facilitate viral infection and replication. In the present study, we found that HSV-1 tegument protein VP22 acts as an inhibitor of cGAS/stimulator of interferon genes (cGAS/STING)-mediated production of interferon (IFN) and its downstream antiviral genes. Our results showed that ectopic expression of VP22 decreased cGAS/STING-mediated IFN-β promoter activation and IFN-β production. Infection with wild-type (WT) HSV-1, but not VP22-deficient virus (ΔVP22), inhibited immunostimulatory DNA (ISD)-induced activation of the IFN signaling pathway. Further study showed that VP22 interacted with cGAS and inhibited the enzymatic activity of cGAS. In addition, stable knockdown of cGAS facilitated the replication of ΔVP22 virus but not the WT. In summary, our findings indicate that HSV-1 VP22 acts as an antagonist of IFN signaling to persistently evade host innate antiviral responses.

Indexed as

Immunity, InnateAnimalsChlorocebus aethiopsCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHEK293 CellsHerpesvirus 1, HumanHumansInterferon-betaMembrane ProteinsNucleotidyltransferasesSignal TransductionSTING ProteinVero CellsViral Structural ProteinscGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate Synthaseherpes simplex virus type 1 protein VP22Interferon-betaMembrane ProteinsNucleotidyltransferasesSTING1 protein, humanSTING ProteinViral Structural ProteinscGASDNA sensingHSV-1VP22

Identifiers

PMID29793952
PMCPMC6052299
OpenAlexW2805015236

What OpenQuestion holds

Textmetadata
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.