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Alberta Institute for Viral Immunology, Department of Medical Microbiology & Immunology, University of Alberta, Edmonton, Alberta T6G 2S2, Canada; Department of Pathology & Molecular Medicine, McMaster University, Hamilton, Ontario L8N 3Z5, Canada
* To whom correspondence should be addressed. Email:
jim.smiley{at}ualberta.ca.
Herpes simplex virus VP16 and ICP0 mutants replicate efficiently in U2OS osteosarcoma cells but are restricted in other cell types. We previously showed that the restrictive phenotype is dominant in a transient cell fusion assay, suggesting that U2OS cells lack an antiviral mechanism present in other cells. Recent data indicate that unscheduled membrane fusion events can activate expression of interferon-stimulated genes (ISGs) in fibroblasts, raising the possibility that our earlier results were due to a fusion-induced antiviral state. However, we show here that the permissive phenotype is also extinguished following fusion with Vero cells in the absence of ISG induction.
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Cell fusion-induced activation of interferon-stimulated genes is not required for restriction of a herpes simplex virus VP16/ICP0 mutant in heterokarya formed between permissive and restrictive cells
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