Evidence map›Paper›PMID 35512649›Full record

ArticleJournal of innate immunity2022

Innate Immune Responses to RSV Infection Facilitated by OGG1, an Enzyme Repairing Oxidatively Modified DNA Base Lesions.

Xu Zheng, Ke Wang, Lang Pan, Wenjing Hao, Yaoyao Xue, Attila Bacsi, Spiros A Vlahopoulos, Zsolt Radak, Tapas K Hazra, Allan R Brasier and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025
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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

13 authors at 3 institutions in 2 countries.

Xu ZhengDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Ke WangDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Lang PanDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Wenjing HaoDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Yaoyao XueDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Attila BacsiDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Spiros A VlahopoulosDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Zsolt RadakDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Tapas K HazraDepartment of Internal Medicine, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Allan R BrasierInstitute for Clinical and Translational Research, University of Wisconsin-Madison School of Medicine and Public Health, Madison, Wisconsin, USA.
Lloyd TannerDepartment of Clinical Sciences Lund, Respiratory Medicine & Allergology, Lund University and Skåne University Hospital, Lund, Sweden.
Xueqing BaDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
Istvan BoldoghDepartment of Microbiology and Immunology, University of Texas Medical Branch at Galveston, Galveston, Texas, USA.
The University of Texas Medical Branch at Galveston · USLund University · SEUniversity of Wisconsin–Madison · US

Funding

Virus, Tissue Culture and ImmunoassayP01AI062885 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI BOLDOGH, ISTVAN STEVEN · 2005 to 2022
$23.9M
Preferential single-strand break repair in the active genes of mammalian cellsR01NS073976 · NINDS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI HAZRA, TAPAS K · 2012 to 2021
$3.3M
NIAID NIH HHS P01 AI062885NINDS NIH HHS R01 NS073976
6 · The paper itself

Abstract

The primary cause of morbidity and mortality from infection with respiratory syncytial virus (RSV) is the excessive innate immune response(s) (IIR) in which reactive oxygen species (ROS) play key role(s). However, the mechanisms for these processes are not fully understood. We hypothesized that expressions of IIR genes are controlled by the ROS-generated epigenetic-like mark 7,8-dihydro-8-oxo(d)guanine (8-oxo(d)Gua) and 8-oxoguanine DNA glycosylase1 (OGG1). Here, we report that ROS not only generates intrahelical 8-oxo(d)Gua, but also enzymatically disables OGG1 in RSV-infected human airway epithelial cells and mouse lungs. OGG1 bound to 8-oxo(d)Gua in gene regulatory sequences promotes expression of IIR genes, and consequently exacerbates lung inflammation, histological changes, and body weight loss of experimental animals. Pharmacological inhibition of OGG1 substrate binding decreased expression of RSV-induced chemokine and cytokines and significantly lessened clinical symptoms. Results of mechanistic studies show that OGG1 binding at 8-oxo(d)Gua promoter regions modulated loading of transcription factors via transient cooperative interactions in RSV-infected lungs and airway epithelial cells. Other base specific DNA repair proteins had no effects. Collectively, this study identifies unprecedented roles of ROS-generated DNA base lesion(s) and cognate repair protein as a determinant of RSV-induced exuberant inflammation. Pharmaceutical inhibition of OGG1 interaction with its DNA substrate may represent a novel strategy in prevention/intervention of respiratory viral infections.

Indexed as

DNA GlycosylasesImmunity, InnateAnimalsDNAHumansMiceDNADNA GlycosylasesOgg1 protein, mouseInnate immune responseOGG1Oxidative DNA base damageRespiratory syncytial virus infection

Identifiers

PMID35512649
PMCPMC9801259
OpenAlexW4229061995

What OpenQuestion holds

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LicenceCC BY-NC
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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.