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Complementation of Vaccinia Virus Deleted of the E3L Gene by Mutants of E3L

1997; Elsevier BV; Volume: 239; Issue: 2 Linguagem: Inglês

10.1006/viro.1997.8881

1096-0341

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

Plant Virus Research Studies

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.