Complementation of vaccinia virus deleted of the E3L gene by mutants of E3L

Teri Shors, Karen Kibler, Kim B. Perkins, Renee Seidler-Wulff, Matthew P. Banaszak, Bertram Jacobs

Research output: Contribution to journalArticlepeer-review

53 Scopus citations

Abstract

Vaccinia virus devoid of its E3L gene is sensitive to treatment of RK- 13 cells with interferon-α and fails to replicate or form plaques in HeLa cells. In order to determine function of the E3L gene, vaccinia virus recombinants were constructed by inserting mutant E3L genes or a gene coding for an alternative dsRNA-binding protein into virus deleted of its wild type E3L gene. Those viruses that expressed proteins that retained dsRNA binding activity were resistant to the effects of interferon in RK-13 cells and could replicate in HeLa cells. Recombinant viruses that expressed E3L mutant proteins which were unable to bind to dsRNA were interferon sensitive in RK- 13 cells and could not replicate in HeLa cells. In addition, a virus that expressed a mutant E3L protein previously characterized as having a low binding affinity for dsRNA exhibited an intermediate phenotype: it was interferon resistant in RK-13 cells but could not replicate in HeLa cells. This work suggests that the E3L gene of vaccinia virus functions primarily as a dsRNA-binding protein in allowing resistance to interferon and in promoting replication in HeLa cells.

Original languageEnglish (US)
Pages (from-to)269-276
Number of pages8
JournalVirology
Volume239
Issue number2
DOIs
StatePublished - Dec 22 1997

ASJC Scopus subject areas

  • Virology

Fingerprint

Dive into the research topics of 'Complementation of vaccinia virus deleted of the E3L gene by mutants of E3L'. Together they form a unique fingerprint.

Cite this