Recombinant myxoma virus lacking all poxvirus ankyrin-repeat proteins stimulates multiple cellular anti-viral pathways and exhibits a severe decrease in virulence

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7 Scopus citations

Abstract

Although the production of single gene knockout viruses is a useful strategy to study viral gene functions, the redundancy of many host interactive genes within a complex viral genome can obscure their collective functions. In this study, a rabbit-specific poxvirus, myxoma virus (MYXV), was genetically altered to disrupt multiple members of the poxviral ankyrin-repeat (ANK-R) protein superfamily, M-T5, M148, M149 and M150. A particularly robust activation of the NF-κB pathway was observed in A549 cells following infection with the complete ANK-R knockout (vMyx-ANKsKO). Also, an increased release of IL-6 was only observed upon infection with vMyx-ANKsKO. In virus-infected rabbit studies, vMyx-ANKsKO was the most extensively attenuated and produced the smallest primary lesion of all ANK-R mutant constructs. This study provides the first insights into the shared functions of the poxviral ANK-R protein superfamily in vitro and in vivo.

Original languageEnglish (US)
Pages (from-to)134-145
Number of pages12
JournalVirology
Volume464-465
Issue number1
DOIs
StatePublished - Sep 2014
Externally publishedYes

Keywords

  • Ankyrin-repeat
  • Interleukin 6
  • M-T5
  • M148
  • M149
  • M150
  • Myxoma virus
  • Myxomatosis
  • Nuclear factor kappa B
  • Poxvirus

ASJC Scopus subject areas

  • Virology

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