Analysis of anti-interferon properties of the herpes simplex virus type I ICP0 protein.
A defining hallmark of the type 1 interferons (IFNs) is their ability to interfere with virus replication. As such, viruses have evolved diverse mechanisms to subvert the antiviral effects of interferons. Herpes simplex virus type 1 (HSV-1) is a large deoxyribonucleic acid virus best known for its ability to cause cold sores in infected individuals. In cultured cells, HSV-1 is relatively resistant to the effects of IFNs. Plaque reduction assays were used to determine that the immediate early HSV-1 gene product ICP0 functions in part to ensure successful replication in the presence of an IFN-induced antiviral response. Northern blot analysis showed that in the absence of ICP0, HSV-1 transcript accumulation is significantly decreased. Finally, nuclear run-on assays demonstrated that ICP0 functions to overcome IFN-induced blocks to virus transcription. The methods used in these studies are described in detail in this section.
Center for Gene Therapeutics, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
Karen
K
Mossman
D000818:Animals; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D006561:Herpes Simplex / Q000276:immunology; D018259:Herpesvirus 1, Human / Q000235:genetics / Q000276:immunology; D006801:Humans; D017874:Immediate-Early Proteins / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D007372:Interferons / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D012367:RNA, Viral / Q000378:metabolism; D014158:Transcription, Genetic; D044767:Ubiquitin-Protein Ligases
D017874:Immediate-Early Proteins; D012367:RNA, Viral; D007372:Interferons; D044767:Ubiquitin-Protein Ligases; C051804:Vmw110 protein, Human herpesvirus 1