Evidence map›Paper›PMID 32636381›Full record

ArticleNature communications2020

Interferon-independent STING signaling promotes resistance to HSV-1 in vivo.

Lívia H Yamashiro, Stephen C Wilson, Huntly M Morrison, Vasiliki Karalis, Jing-Yi J Chung, Katherine J Chen, Helen S Bateup, Moriah L Szpara, Angus Y Lee, Jeffery S Cox and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

111 citing papers in PubMed, 169 citations in OpenAlex.

  1. Review
  2. Article
  3. Lactylation: a novel post-translational modification for cGAS-STING pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  16. Article
  17. Article
  18. Alternative cGAS signaling promotes herpes simplex encephalitis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  19. Article
  20. Article

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

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

11 authors at 5 institutions in 1 country.

Lívia H YamashiroDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Stephen C WilsonDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Huntly M MorrisonDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Vasiliki KaralisDivision of Neurobiology, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Jing-Yi J ChungDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Katherine J ChenDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Helen S BateupDivision of Neurobiology, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.ORCID http://orcid.org/0000-0002-0135-0972
Moriah L SzparaDepartments of Biology and Biochemistry & Molecular Biology, Center for Infectious Disease Dynamics, Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, Pennsylvania, PA, 16801, USA.ORCID http://orcid.org/0000-0001-9859-1678
Angus Y LeeCancer Research Laboratory, University of California, Berkeley, CA, 94720, USA.
Jeffery S CoxDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA.
Russell E VanceDivision of Immunology and Pathogenesis, Department of Molecular and Cell Biology, University of California, Berkeley, CA, 94720, USA. rvance@berkeley.edu.ORCID http://orcid.org/0000-0002-6686-3912
University of California, Berkeley · USHoward Hughes Medical Institute · USBristol-Myers Squibb (United States) · USChan Zuckerberg Initiative (United States) · USPennsylvania State University · US

Funding

Immunology & Pathogenesis Program Training GrantT32AI100829 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI Gregory M Barton, ELLEN A ROBEY · 2012 to 2026
$4.7M
Functional and Structural Dissection of Inflammasome ActivationR37AI075039 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI RUSSELL E VANCE · 2018 to 2026
$3.8M
Specificity and in vivo function of the Naip/Nlrc4 inflammasomesR01AI075039 · NIAID · UNIVERSITY OF CALIFORNIA BERKELEY · PI VANCE, RUSSELL E · 2008 to 2017
$3.6M
Forward genetic prediction and testing of virulence loci in herpes simplex virus 1R01AI132692 · NIAID · PENNSYLVANIA STATE UNIVERSITY, THE · PI SZPARA, MORIAH · 2018 to 2022
$2.3M
Automated High-Throughput, High-Content Confocal/Wide-Field Microscope SystemS10OD021828 · OD · UNIVERSITY OF CALIFORNIA BERKELEY · PI WEST, MARY · 2017 to 2017
$1.0M
A Zeiss LSM 710 confocal microscope for the Biological Imaging Facility at the US10RR026866 · NCRR · UNIVERSITY OF CALIFORNIA BERKELEY · PI RUZIN, STEVEN EARL · 2010 to 2010
$419k
Howard Hughes Medical InstituteNCRR NIH HHS S10 RR026866NIAID NIH HHS R01 AI075039NIAID NIH HHS R01 AI132692NIAID NIH HHS R37 AI075039NIH HHS S10 OD021828
6 · The paper itself

Abstract

The Stimulator of Interferon Genes (STING) pathway initiates potent immune responses upon recognition of DNA. To initiate signaling, serine 365 (S365) in the C-terminal tail (CTT) of STING is phosphorylated, leading to induction of type I interferons (IFNs). Additionally, evolutionary conserved responses such as autophagy also occur downstream of STING, but their relative importance during in vivo infections remains unclear. Here we report that mice harboring a serine 365-to-alanine (S365A) mutation in STING are unexpectedly resistant to Herpes Simplex Virus (HSV)-1, despite lacking STING-induced type I IFN responses. By contrast, resistance to HSV-1 is abolished in mice lacking the STING CTT, suggesting that the STING CTT initiates protective responses against HSV-1, independently of type I IFNs. Interestingly, we find that STING-induced autophagy is a CTT- and TBK1-dependent but IRF3-independent process that is conserved in the STING S365A mice. Thus, interferon-independent functions of STING mediate STING-dependent antiviral responses in vivo.

Indexed as

AnimalsAutophagyFemaleHerpes SimplexHerpesvirus 1, HumanImmune EvasionInterferon Regulatory Factor-3Interferon Type IMacrophagesMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, Mutant StrainsPoint MutationInterferon Regulatory Factor-3Interferon Type IIrf3 protein, mouseMembrane ProteinsSting1 protein, mouseSTING Protein

Identifiers

PMID32636381
PMCPMC7341812
OpenAlexW3039224043

What OpenQuestion holds

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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.