Abstract
The chimeric herpes simplex viruses (HSV) are Δγ₁34.5 vectors encoding the human cytomegalovirus (HCMV) IRS1 or TRS1 genes. They are capable of late viral protein synthesis and are superior to Δγ₁34.5 HSVs in oncolytic activity. The interferon (IFN) response limits efficient HSV gene expression and replication. HCMV TRS1 and IRS1 restore one γ₁34.5 gene function: evasion of IFN-inducible protein kinase R, allowing late viral protein synthesis. Here we show that, unlike wild-type HSV, the chimeric HSV do not restore another γ₁34.5 function, the suppression of early IFN signaling mediated by IFN regulatory factor 3 (IRF3).
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line
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Cytomegalovirus / genetics*
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Gene Expression
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Genetic Vectors / genetics
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Genetic Vectors / immunology
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Genetic Vectors / physiology
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Herpes Simplex / genetics*
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Herpes Simplex / immunology
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Herpes Simplex / metabolism
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Herpes Simplex / virology
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Humans
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Interferon Regulatory Factor-3 / genetics
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Interferon Regulatory Factor-3 / immunology*
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Interferon Regulatory Factor-3 / metabolism
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Interferon-beta / genetics
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Interferon-beta / immunology
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Oncolytic Virotherapy / instrumentation*
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Phosphorylation
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Simplexvirus / genetics
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Simplexvirus / immunology
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Simplexvirus / physiology*
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Viral Proteins / genetics*
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Viral Proteins / immunology
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Viral Proteins / metabolism
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Virus Replication
Substances
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IRF3 protein, human
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Interferon Regulatory Factor-3
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TRS1 protein, Human herpesvirus 5
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Viral Proteins
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Interferon-beta