ArticleVirologica Sinica2023
OGG1 inhibition suppresses African swine fever virus replication.
Article in Virologica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- African swine fever virus DEAD-box helicase D1133L promotes OGG1-driven incision of genomic 8-oxoG via HDAC5 deacetylation.Journal of molecular cell biology · 2026Article
- Resveratrol inhibits African swine fever virus replicationEmerging microbes & infections · 2025Article
- Review
- African swine fever virus MGF505-3R facilitates ferroptosis to restrict TBK1-IRF3 pathway.Microbiology spectrum · 2025Article
- African swine fever virus A151R downregulates cGAS-STING-mediated IFN-β production by promoting lipid peroxidation through ferritinophagy-induced ferroptosis.Cellular and molecular life sciences : CMLS · 2025Article
- African swine fever virus enhances viral replication by increasing intracellular reduced glutathione levels, which suppresses stress granule formation.Veterinary research · 2024Article
- NEIL1 block IFN-β production and enhance vRNP function to facilitate influenza A virus proliferation.Npj viruses · 2024Article
- 8-Oxoguanine DNA Glycosylase1 conceals oxidized guanine in nucleoprotein-associated RNA of respiratory syncytial virus.PLoS pathogens · 2024Article
- The potential for OGG1 inhibition to be a therapeutic strategy for pulmonary diseases.Expert opinion on therapeutic targets · 2024Review
- Epigenetic control of type III interferon expression by 8-oxoguanine and its reader 8-oxoguanine DNA glycosylase1.Frontiers in immunology · 2023Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
African swine fever virus (ASFV) is an important pathogen that causes a highly contagious and lethal disease in swine, for which neither a vaccine nor treatment is available. The DNA repair enzyme 8-oxoguanine DNA glycosylase 1 (OGG1), which excises the oxidative base lesion 8-oxo-7,8-dihydroguanine (8-oxoG), has been linked to the pathogenesis of different diseases associated with viral infections. However, the role of OGG1-base excision repair (BER) in ASFV infection has been poorly investigated. Our study aimed to characterize the alteration of host reactive oxygen species (ROS) and OGG1 and to analyse the role of OGG1 in ASFV infection. We found that ASFV infection induced high levels and dynamic changes in ROS and 8-oxoG and consistently increased the expression of OGG1. Viral yield, transcription level, and protein synthesis were reduced in ASFV-infected primary alveolar macrophages (PAMs) treated by TH5487 or SU0268 inhibiting OGG1. The expression of BER pathway associated proteins of ASFV was also suppressed in OGG1-inhibited PAMs. Furthermore, OGG1 was found to negatively regulate interferon β (IFN-β) production during ASFV infection and IFN-β could be activated by OGG1 inhibition with TH5487 and SU0268, which blocked OGG1 binding to 8-oxoG. Additionally, the interaction of OGG1 with viral MGF360-14-L protein could disturb IFN-β production to further affect ASFV replication. These results suggest that OGG1 plays the crucial role in successful viral infection and OGG1 inhibitors SU0268 or TH5487 could be used as antiviral agents for ASFV infection.
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