@article{mbs:/content/journal/jgv/10.1099/0022-1317-73-11-2955, author = "Weber, Peter C. and Kenny, Joseph J. and Wigdahl, Brian", title = "Antiviral properties of a dominant negative mutant of the herpes simplex virus type 1 regulatory protein ICP0", journal= "Journal of General Virology", year = "1992", volume = "73", number = "11", pages = "2955-2961", doi = "https://doi.org/10.1099/0022-1317-73-11-2955", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/0022-1317-73-11-2955", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "Dominant negative or trans-dominant mutants of viral proteins represent a new and exciting potential approach to antiviral therapy. Unfortunately, the extreme specificity of a given dominant negative mutant limits its general utility in treating a broad spectrum of viral diseases, since it can typically interfere with the activity of only a single viral polypeptide encoded by a single virus. However, it seems likely that dominant negative mutants of promiscuous viral trans-activator proteins, which by definition would repress rather than activate gene expression, should be able to inhibit infectious virus production for a number of different viruses. One such dominant negative mutant, derived from the herpes simplex virus type 1 (HSV-1) regulatory protein ICP0, was found previously to behave as a powerful repressor of gene expression from an assortment of HSV-1 and non-HSV-1 promoters in transient expression assays. In the present study, this ICP0 mutant was found to be capable of inhibiting the replication of both HSV-1 and a completely unrelated virus, human immunodeficiency virus, in cell culture. The properties of this dominant negative mutant indicate that it may have potential as a means of treating diseases caused by a number of DNA and RNA viruses. Moreover, a truncated form of ICP0 which can hypothetically be created by alternative splicing was found to possess similar inhibitory capabilities, suggesting that a virus-encoded version of this dominant negative mutant may play a role in down-regulating HSV-1 gene expression during infection in vivo.", }