The Orf virus E3L homologue is able to complement deletion of the vaccinia virus E3L gene in vitro but not in vivo

Sangeetha Vijaysri, Latha Talasela, Andrew A. Mercer, Colin J. Mcinnes, Bertram Jacobs, Jeffrey Langland

Research output: Contribution to journalArticle

20 Scopus citations

Abstract

Orf virus (OV), the prototypic parapoxvirus, is resistant to the effects of interferon (IFN) and this function of OV has been mapped to the OV20.0L gene. The protein product of this gene shares 31% amino acid identity to the E3L-encoded protein of vaccinia virus (VV) that is required for the broad host range and IFN-resistant phenotype of VV in cells in culture and for virulence of the virus in vivo. In this study we investigated whether the distantly related OV E3L homologue could complement the deletion of E3L in VV. The recombinant VV (VV/ORF-E3L) expressing the OV E3L homologue in place of VV E3L was indistinguishable from wt VV in its cell-culture phenotype. But VV/ORF-E3L was over a 1000-fold less pathogenic than wt VV (LD50 > 5 × 106 PFU, compared to LD50 of wtVV = 4 × 10 3 PFU) following intranasal infection of mice. While wt VV spread to the lungs and brain and replicated to high titers in the brain of infected mice, VV/ORF-E3L could not be detected in the lungs or brain following intranasal infection. VV/ORF-E3L was at least 100,000-fold less pathogenic than wt VV on intracranial injection. Domain swap experiments demonstrate that the difference in pathogenesis maps to the C-terminal domain of these proteins. This domain has been shown to be required for the dsRNA binding function of the VV E3L.

Original languageEnglish (US)
Pages (from-to)305-314
Number of pages10
JournalVirology
Volume314
Issue number1
DOIs
StatePublished - Sep 15 2003

Keywords

  • E3L
  • OV20.0L
  • Orf virus
  • Vaccinia
  • Virulence
  • dsRNA-binding protein

ASJC Scopus subject areas

  • Virology

Fingerprint Dive into the research topics of 'The Orf virus E3L homologue is able to complement deletion of the vaccinia virus E3L gene in vitro but not in vivo'. Together they form a unique fingerprint.

  • Cite this