title: Initial characterization of vaccinia virus B4 suggests a role in virus spread.
abstract: Currently, little is known about the ankyrin/F-box protein B4. Here, we report that B4R-null viruses exhibited reduced plaque size in tissue culture, and decreased ability to spread, as assessed by multiple-step growth analysis. Electron microscopy indicated that B4R-null viruses still formed mature and extracellular virions; however, there was a slight decrease of virions released into the media following deletion of B4R. Deletion of B4R did not affect the ability of the virus to rearrange actin; however, VACV811, a large vaccinia virus deletion mutant missing 55 open reading frames, had decreased ability to produce actin tails. Using ectromelia virus, a natural mouse pathogen, we demonstrated that virus devoid of EVM154, the B4R homolog, showed decreased spread to organs and was attenuated during infection. This initial characterization suggests that B4 may play a role in virus spread, and that other unidentified mediators of actin tail formation may exist in vaccinia virus.
authors.affiliation: Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
authors.forename: Kristin
authors.initials: K
authors.lastname: Burles
authors.affiliation: Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
authors.forename: Chad R
authors.initials: CR
authors.lastname: Irwin
authors.affiliation: Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
authors.forename: Robyn-Lee
authors.initials: RL
authors.lastname: Burton
authors.affiliation: Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
authors.forename: Jill
authors.initials: J
authors.lastname: Schriewer
authors.affiliation: Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2.
authors.forename: David H
authors.initials: DH
authors.lastname: Evans
authors.affiliation: Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, St. Louis, MO, USA.
authors.forename: R Mark
authors.initials: RM
authors.lastname: Buller
authors.affiliation: Li Ka Shing Institute of Virology, Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, Alberta, Canada T6G 2S2. Electronic address: michele.barry@ualberta.ca.
authors.forename: Michele
authors.initials: M
authors.lastname: Barry
mesh_terms: D000825:Animal Structures / Q000821:virology; D000818:Animals; D004481:Ectromelia virus / Q000235:genetics / Q000472:pathogenicity; D004482:Ectromelia, Infectious / Q000473:pathology / Q000821:virology; D005260:Female; D017353:Gene Deletion; D051379:Mice; D008810:Mice, Inbred C57BL; D046529:Microscopy, Electron, Transmission; D014616:Vaccinia virus / Q000235:genetics / Q000254:growth & development* / Q000648:ultrastructure; D019562:Viral Load; D010948:Viral Plaque Assay; D014764:Viral Proteins / Q000235:genetics / Q000378:metabolism*; D014771:Virion / Q000648:ultrastructure; D014774:Virulence
chemical_list: D014764:Viral Proteins
keywords: Actin tails; B4R; Ectromelia virus; Poxvirus; Vaccinia virus; Virulence; Virus plaque; Virus spread