ArticleVirus research2023
ZNF219, a novel transcriptional repressor, inhibits transcription of the prototype foamy virus by interacting with the viral LTR promoter.
Article in Virus research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Tissue-resident immune cells drive genetic risk in autoimmune and lung diseases.Nature immunology · 2026Article
- ZNF219 inhibits porcine epidemic diarrhea virus by degrading viral S2 protein.Virologica Sinica · 2026Article
- VCY mediates inhibition of PFV replication via interaction with the transcription activator Tas.Journal of virology · 2025Article
- Integration of bioinformatics analysis reveals ZNF248 as a potential prognostic and immunotherapeutic biomarker for LIHC: machine learning and experimental evidence.American journal of cancer research · 2024Article
- TheViruses · 2023Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prototype foamy virus (PFV) is an ancient retrovirus that infects humans with persistent latent infections and non-pathogenic consequences. Lifelong latent PFV infections can be caused by restrictive factors in the host. However, the molecular mechanisms underlying host cell regulation during PFV infection are not fully understood. The aim of the study was to investigate whether a zinc finger protein (ZFP), ZNF219, as a transcription factor, can regulate the transcriptional activity of the viral promoter. Here, using transcriptome sequencing, we found that ZNF219, is downregulated in PFV infected cells and that ZNF219 suppresses viral replication by targeting the viral 5'LTR promoter region to repress its transcription. We also found that PFV infection induced abnormal expression of miRNAs targeting the ZNF219-3'UTR to downregulate ZNF219 expression. These findings indicated that ZNF219 may be a potent antiviral factor for suppressing PFV infection, and may shed light on the mechanism of virus-host interactions.
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