ArticleViruses2015
Human Pirh2 is a novel inhibitor of prototype foamy virus replication.
Article in Viruses, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- PFV Tas protein recruits hnRNPF to promote the splicing of tas/bet pre-mRNA.Cell & bioscience · 2026Article
- VCY mediates inhibition of PFV replication via interaction with the transcription activator Tas.Journal of virology · 2025Article
- SAP30 deacetylates the Tas protein to inhibit PFV replication.Cell & bioscience · 2025Article
- PREB inhibits the replication of prototype foamy virus by affecting its transcription.Virology journal · 2023Article
- TheViruses · 2023Article
- ZNF219, a novel transcriptional repressor, inhibits transcription of the prototype foamy virus by interacting with the viral LTR promoter.Virus research · 2023Article
- Mechanisms of Innate Immune Sensing of HTLV-1 and Viral Immune Evasion.Pathogens (Basel, Switzerland) · 2023Review
- Article
- Review
- SGK1, a Serine/Threonine Kinase, Inhibits Prototype Foamy Virus Replication.Microbiology spectrum · 2022Article
- The Role of E3 Ligase Pirh2 in Disease.Cells · 2022Review
- Trim28 acts as restriction factor of prototype foamy virus replication by modulating H3K9me3 marks and destabilizing the viral transactivator Tas.Retrovirology · 2021Article
- Foamy Viruses, Bet, and APOBEC3 Restriction.Viruses · 2021Review
- Novel Host Protein TBC1D16, a GTPase Activating Protein of Rab5C, Inhibits Prototype Foamy Virus Replication.Frontiers in immunology · 2021Article
- Prototype foamy virus downregulates RelB expression to facilitate viral replication.FEBS open bio · 2020Article
- Inhibition of spumavirus gene expression by PHF11.PLoS pathogens · 2020Article
- Lnc-RP5 Regulates the miR-129-5p/Notch1/PFV Internal Promoter Axis to Promote the Expression of the Prototype Foamy Virus Transactivator Tas.Virologica Sinica · 2020Article
- Review
- Functional characterization of the bovine foamy virus miRNA expression cassette and its dumbbell-shaped pri-miRNA.Virus genes · 2018Article
- Prototype foamy virus elicits complete autophagy involving the ER stress-related UPR pathway.Retrovirology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prototype foamy virus (PFV) is a member of the unconventional and nonpathogenic retroviruses. PFV causes lifelong chronic infections, which are partially attributable to a number of host cell factors that restrict viral replication. Herein, we identified human p53-induced RING-H2 protein (Pirh2) as a novel inhibitor of prototype foamy virus. Overexpression of Pirh2 decreased the replication of PFV, whereas knockdown of Pirh2 with specific siRNA increased PFV replication. Dual-luciferase assays and coimmunoprecipitation demonstrated that Pirh2 negatively influences the Tas-dependent transcriptional activation of the PFV long terminal repeat (LTR) and internal promoter (IP) by interacting with the transactivator Tas and down-regulating its expression. In addition, the viral inhibitory function of Pirh2 is N-terminal and RING domain dependent. Together, these results indicated that Pirh2 suppresses PFV replication by negatively impacting its transactivator Tas and the transcription of two viral promoters, which may contribute to the latency of PFV infection.
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What OpenQuestion holds
Registered trials
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.