ArticlePLoS pathogens2020
Zinc-finger antiviral protein (ZAP) is a restriction factor for replication of modified vaccinia virus Ankara (MVA) in human cells.
Article in PLoS pathogens, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 46 citations in OpenAlex.
- A feline coronavirus nucleocapsid protein disrupts ZC3HAV1-viral RNA association to counteract host RNA-level restriction.PLoS pathogens · 2026Article
- The ISG Atlas: a loss-of-function analysis characterizes antiviral properties of interferon stimulated genes.Nature communications · 2026Article
- Poxvirus A52 protein subverts autophagy flux by blocking autophagosome-lysosome fusion to promote viral replication.PLoS pathogens · 2026Article
- Lycorine Derivative Inhibits SARS-CoV-2 Replication by Reducing -1 Programmed Ribosomal Frameshifting via Targeting ZAP.MedComm · 2026Article
- Poxvirus attack of antiviral defense pathways unleashes an effector-triggered NF-κB response.Science (New York, N.Y.) · 2026Article
- Poxvirus Host-Range Determinants: SAMD9/9L and Beyond.Annual review of virology · 2025Review
- The vaccinia virus protein, C16, promotes the ubiquitylation and relocalization of the antiviral E3 ubiquitin-ligase, TRIM25.Journal of virology · 2025Article
- Modulation of host gene expression by the zinc finger antiviral protein.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Catch me if you can: viral nucleic acids to host sensors.Frontiers in immunology · 2025Review
- The Human Monkeypox Virus and Host Immunity: Emerging Diagnostic and Therapeutic Challenges.Infectious disorders drug targets · 2025Review
- Evolutionary analysis of ZAP and its cofactors identifies intrinsically disordered regions as central elements in host-pathogen interactions.Computational and structural biotechnology journal · 2024Article
- The nuclear localization signal of monkeypox virus protein P2 orthologue is critical for inhibition of IRF3-mediated innate immunity.Emerging microbes & infections · 2024Article
- ZC3HAV1 facilitates STING activation and enhances inflammation.Communications biology · 2024Article
- Abortive Infection of Animal Cells: What Goes Wrong.Annual review of virology · 2024Review
- Versatility of the Zinc-Finger Antiviral Protein (ZAP) As a Modulator of Viral Infections.International journal of biological sciences · 2024Review
- Zoonotic and Zooanthroponotic Potential of Monkeypox.Advances in experimental medicine and biology · 2024Review
- Antiviral Activity of Zinc Finger Antiviral Protein (ZAP) in Different Virus Families.Pathogens (Basel, Switzerland) · 2023Review
- Quantitative proteomics defines mechanisms of antiviral defence and cell death during modified vaccinia Ankara infection.Nature communications · 2023Article
- Human FAM111A inhibits vaccinia virus replication by degrading viral protein I3 and is antagonized by poxvirus host range factor SPI-1.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modified vaccinia virus Ankara (MVA) is an approved smallpox vaccine and a promising vaccine vector for other pathogens as well as for cancer therapeutics with more than 200 current or completed clinical trials. MVA was derived by passaging the parental Ankara vaccine virus hundreds of times in chick embryo fibroblasts during which it lost the ability to replicate in human and most other mammalian cells. Although this replication deficiency is an important safety feature, the genetic basis of the host restriction is not understood. Here, an unbiased human genome-wide RNAi screen in human A549 cells revealed that the zinc-finger antiviral protein (ZAP), previously shown to inhibit certain RNA viruses, is a host restriction factor for MVA, a DNA virus. Additional studies demonstrated enhanced MVA replication in several human cell lines following knockdown of ZAP. Furthermore, CRISPR-Cas9 knockout of ZAP in human A549 cells increased MVA replication and spread by more than one log but had no effect on a non-attenuated strain of vaccinia virus. The intact viral C16 protein, which had been disrupted in MVA, antagonized ZAP by binding and sequestering the protein in cytoplasmic punctate structures. Studies aimed at exploring the mechanism by which ZAP restricts MVA replication in the absence of C16 showed that knockout of ZAP had no discernible effect on viral DNA or individual mRNA or protein species as determined by droplet digital polymerase chain reaction, deep RNA sequencing and mass spectrometry, respectively. Instead, inactivation of ZAP reduced the number of aberrant, dense, spherical particles that typically form in MVA-infected human cells, suggesting that ZAP has a novel role in interfering with a late step in the assembly of infectious MVA virions in the absence of the C16 protein.
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