ArticleJournal of virology2013
ZAP inhibits murine gammaherpesvirus 68 ORF64 expression and is antagonized by RTA.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- Host ZAP activity correlates with the levels of CpG suppression in primate lentiviruses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Evolutionary analysis of ZAP and its cofactors identifies intrinsically disordered regions as central elements in host-pathogen interactions.Computational and structural biotechnology journal · 2024Article
- ZNF283, a Krüppel-associated box zinc finger protein, inhibits RNA synthesis of porcine reproductive and respiratory syndrome virus by interacting with Nsp9 and Nsp10.Veterinary research · 2024Article
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Antiviral Activity of Zinc Finger Antiviral Protein (ZAP) in Different Virus Families.Pathogens (Basel, Switzerland) · 2023Review
- Strain-Dependent Restriction of Human Cytomegalovirus by Zinc Finger Antiviral Proteins.Journal of virology · 2023Article
- RNF213 modulates γ-herpesvirus infection and reactivation via targeting the viral Replication and Transcription Activator.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- NAD+-consuming enzymes in immune defense against viral infection.The Biochemical journal · 2021Review
- Does the Zinc Finger Antiviral Protein (ZAP) Shape the Evolution of Herpesvirus Genomes?Viruses · 2021Review
- Interferon-Induced HERC5 Inhibits Ebola Virus Particle Production and Is Antagonized by Ebola Glycoprotein.Cells · 2021Article
- The impact of PARPs and ADP-ribosylation on inflammation and host-pathogen interactions.Genes & development · 2020Review
- The role of ZAP and OAS3/RNAseL pathways in the attenuation of an RNA virus with elevated frequencies of CpG and UpA dinucleotides.Nucleic acids research · 2019Article
- Article
- Inhibition of Japanese encephalitis virus infection by the host zinc-finger antiviral protein.PLoS pathogens · 2018Article
- Zinc Finger-Containing Cellular Transcription Corepressor ZBTB25 Promotes Influenza Virus RNA Transcription and Is a Target for Zinc Ejector Drugs.Journal of virology · 2017Article
- The Short Form of the Zinc Finger Antiviral Protein Inhibits Influenza A Virus Protein Expression and Is Antagonized by the Virus-Encoded NS1.Journal of virology · 2017Article
- Herpes simplex virus 1 UL41 protein abrogates the antiviral activity of hZAP by degrading its mRNA.Virology journal · 2015Article
- Review
- The Broad-Spectrum Antiviral Protein ZAP Restricts Human Retrotransposition.PLoS genetics · 2015Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc finger antiviral protein (ZAP) is an interferon-inducible host antiviral factor that specifically inhibits the replication of certain viruses, including HIV-1 and Ebola virus. ZAP functions as a dimer formed through intermolecular interactions of its N-terminal tails. ZAP binds directly to specific viral mRNAs and inhibits their expression by repressing translation and/or promoting degradation of the target mRNA. ZAP is not a universal antiviral factor, since some viruses grow normally in ZAP-expressing cells. It is not fully understood what determines whether a virus is susceptible to ZAP. We explored the interaction between ZAP and murine gammaherpesvirus 68 (MHV-68), whose life cycle has latent and lytic phases. We previously reported that ZAP inhibits the expression of M2, which is expressed mainly in the latent phase, and regulates MHV-68 latency in cultured cells. Here, we report that ZAP inhibits the expression of ORF64, a tegument protein that is expressed in the lytic phase and is essential for lytic replication. MHV-68 infection induced ZAP expression. However, ZAP did not inhibit lytic replication of MHV-68. We provide evidence showing that the antiviral activity of ZAP is antagonized by MHV-68 RTA, a critical viral transactivator expressed in the lytic phase. We further show that RTA inhibits the antiviral activity of ZAP by disrupting the N-terminal intermolecular interaction of ZAP. Our results provide an example of how a virus can escape ZAP-mediated immunity.
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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.