title: Analysis of host response modifier ORFs of ectromelia virus, the causative agent of mousepox.
abstract: From the right-hand end of the ectromelia virus (strain Moscow) genome, 32318 bps have been sequenced, and characterized to include a total of 18 open reading frames (ORFs) and six regions which apparently no longer code for functional proteins. At least six of the ORFs appear to be involved in blocking the inflammatory/immune host response to infection, and therefore probably contribute significantly to the virulence of this virus in its natural host, the mouse. One of these genes encoded an isolog of the poxvirus chemokine binding protein, and was shown to be the most abundant protein secreted from ectromelia virus infected cells. Two regions were found to have significant similarity to poxvirus genes encoding tumor necrosis factor (TNF) binding proteins. Both are distinct from cytokine response modifier (crm)B and crmC but only one is predicted to encode a functional TNF binding protein. A novel similarity between the C-terminal domain of poxvirus TNF binding proteins and several other poxvirus proteins is also presented. The results are discussed in the context of ectromelia virus pathogenesis of mice.
authors.affiliation: Department of Molecular Microbiology and Immunology, Saint Louis University Health Sciences Center, 1402 South Grand Boulevard, St. Louis, MO 63104, USA.
authors.forename: N
authors.initials: N
authors.lastname: Chen
authors.forename: R M
authors.initials: RM
authors.lastname: Buller
authors.forename: E M
authors.initials: EM
authors.lastname: Wall
authors.forename: C
authors.initials: C
authors.lastname: Upton
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D000956:Antigens, Viral / Q000032:analysis; D002460:Cell Line; D004251:DNA Transposable Elements; D004481:Ectromelia virus / Q000737:chemistry / Q000235:genetics* / Q000472:pathogenicity; D004482:Ectromelia, Infectious / Q000821:virology*; D005260:Female; D016679:Genome, Viral; D006023:Glycoproteins / Q000235:genetics; D006801:Humans; D007150:Immunohistochemistry; D007155:Immunologic Factors / Q000235:genetics*; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008805:Mice, Inbred A; D008969:Molecular Sequence Data; D016366:Open Reading Frames; D019707:Receptors, Chemokine / Q000235:genetics; D017471:Receptors, Interferon / Q000235:genetics; D017472:Receptors, Interleukin-1 / Q000235:genetics; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics; D016415:Sequence Alignment; D017384:Sequence Deletion; D015843:Serpins / Q000235:genetics; D017193:Skin Diseases, Viral / Q000662:veterinary; D014764:Viral Proteins / Q000235:genetics; D014774:Virulence
chemical_list: D000956:Antigens, Viral; D004251:DNA Transposable Elements; D006023:Glycoproteins; D007155:Immunologic Factors; D008565:Membrane Proteins; D019707:Receptors, Chemokine; D017471:Receptors, Interferon; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D015843:Serpins; D014764:Viral Proteins