title: Truncation of gene F5L partially masks rescue of vaccinia virus strain MVA growth on mammalian cells by restricting plaque size.
abstract: Modified vaccinia virus Ankara (MVA) is a candidate vaccine vector that is severely attenuated due to mutations acquired during several hundred rounds of serial passage in vitro. A previous study used marker rescue to produce a set of MVA recombinants with improved replication on mammalian cells. Here, we extended the characterization of these rescued MVA strains and identified vaccinia virus (VACV) gene F5L as a determinant of plaque morphology but not replication in vitro. F5 joins a growing group of VACV proteins that influence plaque formation more strongly than virus replication and which are disrupted in MVA. These defective genes in MVA confound the interpretation of marker rescue experiments designed to map mutations responsible for the attenuation of this important VACV strain.
authors.affiliation: Division of Biomedical Science and Biochemistry, Research School of Biology, Australian National University, Canberra, ACT, Australia.
authors.forename: Bianca M
authors.initials: BM
authors.lastname: Dobson
authors.affiliation: Division of Biomedical Science and Biochemistry, Research School of Biology, Australian National University, Canberra, ACT, Australia.
authors.forename: David C
authors.initials: DC
authors.lastname: Tscharke
mesh_terms: D000818:Animals; D002460:Cell Line; D006801:Humans; D014616:Vaccinia virus / Q000235:genetics* / Q000254:growth & development* / Q000502:physiology; D010948:Viral Plaque Assay; D014764:Viral Proteins / Q000235:genetics* / Q000378:metabolism*; D014779:Virus Replication
chemical_list: D014764:Viral Proteins