Role of the vaccinia virus E3L and K3L gene products in rescue of VSV and EMCV from the effects of IFN-α

Scott T. Shors, Elizabeth Beattie, Enzo Paoletti, James Tartaglia, Bertram Jacobs

Research output: Contribution to journalArticlepeer-review

41 Scopus citations

Abstract

Vaccinia virus (VV) has been shown to be relatively resistant to the antiviral effects of interferon-α (IFN-α) and to rescue replication of IFN- sensitive viruses, such as encephalomyocarditis virus (EMCV) and vesicular stomatitis virus (VSV), from the antiviral effects of IFN. The E3L and K3L gene products have been implicated in the IFN resistance of VV. We have investigated the role that these VV-encoded functions play in the rescue of VSV and EMCV from the effects of IFN. Transient expression of the E3L open reading frame (ORF) was sufficient to rescue VSV but not EMCV from the IFN- induced antiviral state. Rescue of VSV by mutants of E3L correlated with the ability of the mutated E3L gene products to bind dsRNA. Conversely, transient expression of the K3L ORF was sufficient to partially rescue EMCV but not VSV from the effects of IFN. Results with VV deleted of either the K3L or E3L ORFs were consistent with results obtained by transient expression of these genes. These results demonstrate that the VV E3L gene products are likely responsible for the VV-mediated rescue of VSV from the effects of IFN and the K3L gene product is likely at least partly responsible for rescue of EMCV.

Original languageEnglish (US)
Pages (from-to)721-729
Number of pages9
JournalJournal of Interferon and Cytokine Research
Volume18
Issue number9
DOIs
StatePublished - Sep 1998

ASJC Scopus subject areas

  • Immunology
  • Cell Biology
  • Virology

Fingerprint

Dive into the research topics of 'Role of the vaccinia virus E3L and K3L gene products in rescue of VSV and EMCV from the effects of IFN-α'. Together they form a unique fingerprint.

Cite this