ArticleNature communications2023
The DNA glycosylase NEIL2 is protective during SARS-CoV-2 infection.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Integrative Genomics Identifies Candidate Genes Underlying Trypanotolerance in Hybrid African Cattle.Evolutionary applications · 2026Article
- Chemical Switching: A Concept Inspired by Strategies from Biocatalysis and Organocatalysis.Chembiochem : a European journal of chemical biology · 2025Review
- Low levels of DNA repair enzyme NEIL2 May exacerbate inflammation and genomic damage in subjects with stable COPD and during severe exacerbations.Respiratory research · 2025Article
- Characterization of moyamoya disease molecular subtypes through disulfidptosis‑related genes and immune landscape analysis.Experimental and therapeutic medicine · 2025Article
- DNA repair and disease: insights from the human DNA glycosylase NEIL family.Experimental & molecular medicine · 2025Review
- NEIL1 block IFN-β production and enhance vRNP function to facilitate influenza A virus proliferation.Npj viruses · 2024Article
- Integrating spatial transcriptomics and single-cell RNA-sequencing reveals the alterations in epithelial cells during nodular formation in benign prostatic hyperplasia.Journal of translational medicine · 2024Article
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Authors and funding
23 authors at 5 institutions in 2 countries.
Funding
Abstract
SARS-CoV-2 infection-induced aggravation of host innate immune response not only causes tissue damage and multiorgan failure in COVID-19 patients but also induces host genome damage and activates DNA damage response pathways. To test whether the compromised DNA repair capacity of individuals modulates the severity of COVID-19 infection, we analyze DNA repair gene expression in publicly available patient datasets and observe a lower level of the DNA glycosylase NEIL2 in the lungs of severely infected COVID-19 patients. This observation of lower NEIL2 levels is further validated in infected patients, hamsters and ACE2 receptor-expressing human A549 (A549-ACE2) cells. Furthermore, delivery of recombinant NEIL2 in A549-ACE2 cells shows decreased expression of proinflammatory genes and viral E-gene, as well as lowers the yield of viral progeny compared to mock-treated cells. Mechanistically, NEIL2 cooperatively binds to the 5'-UTR of SARS-CoV-2 genomic RNA to block viral protein synthesis. Collectively, these data strongly suggest that the maintenance of basal NEIL2 levels is critical for the protective response of hosts to viral infection and disease.
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