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.
Mossman
Karen
K
Center for Gene Therapeutics, Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada.
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