ArticleJournal of virology2010
Introduction of the six major genomic deletions of modified vaccinia virus Ankara (MVA) into the parental vaccinia virus is not sufficient to reproduce an MVA-like phenotype in cell culture and in mice.
Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.
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Who cites it
36 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Viral vector-based influenza vaccines.Human vaccines & immunotherapeutics · 2016Pooled it
- STING-mediated antiviral response: insights into MVA replication control in avian cells.Microbiology spectrum · 2025Article
- Differences in Mpox and Vaccinia Immunity Induced by Non-Replicating and Replicating Vaccinia-Based Vaccines.Vaccines · 2025Article
- Understanding the performance of HIV-1 viral vector vaccines: adenovirus and poxvirus case studies.Frontiers in immunology · 2025Review
- Efficacy and immunogenicity of rKVAC85B in a BCG prime-boost regimen against H37Rv and HN878 Mycobacterium tuberculosis strains.PloS one · 2025Article
- Expression of an Efficient Selection Marker Out of a Duplicated Site in the ITRs of a Modified Vaccinia Virus Ankara (MVA).Vaccines · 2024Article
- Poxvirus Recombination.Pathogens (Basel, Switzerland) · 2022Review
- Nanopore sequencing and de novo assembly of a misidentified Camelpox vaccine reveals putative epigenetic modifications and alternate protein signal peptides.Scientific reports · 2021Article
- Review
- Repair of a previously uncharacterized second host-range gene contributes to full replication of modified vaccinia virus Ankara (MVA) in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Efficient Induction of Cytotoxic T Cells by Viral Vector Vaccination Requires STING-Dependent DC Functions.Frontiers in immunology · 2020Article
- SPI-1 is a missing host-range factor required for replication of the attenuated modified vaccinia Ankara (MVA) vaccine vector in human cells.PLoS pathogens · 2019Article
- The Virulence of Different Vaccinia Virus Strains Is Directly Proportional to Their Ability To Downmodulate Specific Cell-Mediated Immune CompartmentsJournal of virology · 2019Article
- CRISPR/Cas9-Advancing Orthopoxvirus Genome Editing for Vaccine and Vector Development.Viruses · 2018Review
- Hazard Characterization of Modified Vaccinia Virus Ankara Vector: What Are the Knowledge Gaps?Viruses · 2017Review
- Article
- A systemic macrophage response is required to contain a peripheral poxvirus infection.PLoS pathogens · 2017Article
- Recombinant Modified Vaccinia Virus Ankara Generating Ebola Virus-Like Particles.Journal of virology · 2017Article
- Redundancy complicates the definition of essential genes for vaccinia virus.The Journal of general virology · 2015Article
- The evolution of poxvirus vaccines.Viruses · 2015Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Modified vaccinia virus Ankara (MVA) has a highly restricted host range in cell culture and is apathogenic in vivo. MVA was derived from the parental chorioallantois vaccinia virus Ankara (CVA) by more than 570 passages in chicken embryo fibroblast (CEF) cells. During CEF cell passaging, six major deletions comprising 24,668 nucleotides occurred in the CVA genome. We have cloned both the MVA and the parental CVA genome as bacterial artificial chromosomes (BACs) and have sequentially introduced the six major MVA deletions into the cloned CVA genome. Reconstituted mutant CVA viruses containing up to six major MVA deletions showed no detectable replication restriction in 12 of 14 mammalian cell lines tested; the exceptions were rabbit cell lines RK13 and SIRC. In mice, CVA mutants with up to three deletions showed slightly enhanced virulence, suggesting that gene deletion in replicating vaccinia virus (VACV) can result in gain of fitness in vivo. CVA mutants containing five or all six deletions were still pathogenic, with a moderate degree of attenuation. Deletion V was mainly responsible for the attenuated phenotype of these mutants. In conclusion, loss or truncation of all 31 open reading frames in the six major deletions is not sufficient to reproduce the specific MVA phenotype of strong attenuation and highly restricted host range. Mutations in viral genes outside or in association with the six major deletions appear to contribute significantly to this phenotype. Host range restriction and avirulence of MVA are most likely a cooperative effect of gene deletions and mutations involving the major deletions.
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