title: Ectromelia virus N1L is essential for virulence but not dissemination in a classical model of mousepox.
abstract: Mousepox is caused by the orthopoxvirus ectromelia virus (ECTV), and is thought to be transmitted via skin abrasions. We studied the ECTV virulence factor N1 following subcutaneous infection of mousepox-susceptible BALB/c mice. In this model, ECTV lacking N1L gene was attenuated more than 1000-fold compared with wild-type virus and replication was profoundly reduced as early as four days after infection. However, in contrast to data from an intranasal model, N1 protein was not required for virus dissemination. Further, neither T cell nor cytokine responses were enhanced in the absence of N1. Together with the early timing of reduced virus titres, this suggests that in a cutaneous model, N1 exerts its function at the level of infected cells or in the inhibition of the very earliest effectors of innate immunity.
authors.affiliation: Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia. Electronic address: carolrezende@gmail.com.
authors.forename: Carolina R
authors.initials: CR
authors.lastname: Melo-Silva
authors.affiliation: Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
authors.forename: David C
authors.initials: DC
authors.lastname: Tscharke
authors.affiliation: Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
authors.forename: Mario
authors.initials: M
authors.lastname: Lobigs
authors.affiliation: Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
authors.forename: Aulikki
authors.initials: A
authors.lastname: Koskinen
authors.affiliation: Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia; Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
authors.forename: Arno
authors.initials: A
authors.lastname: Müllbacher
authors.affiliation: Department of Emerging Pathogens and Vaccines, The John Curtin School of Medical Research, Australian National University, Canberra ACT, Australia.
authors.forename: Matthias
authors.initials: M
authors.lastname: Regner
mesh_terms: D000818:Animals; D004481:Ectromelia virus / Q000502:physiology*; D004482:Ectromelia, Infectious / Q000821:virology*; D054884:Host-Pathogen Interactions; D051379:Mice; D019562:Viral Load; D014764:Viral Proteins / Q000235:genetics* / Q000378:metabolism; D014774:Virulence; D037521:Virulence Factors / Q000235:genetics / Q000378:metabolism; D014779:Virus Replication
chemical_list: D014764:Viral Proteins; D037521:Virulence Factors
keywords: Ectromelia virus; N1L; Poxvirus; Virus-host interaction