Abstract
Herpes simplex viruses lacking the virion host shutoff function (Δvhs) are avirulent and hypersensitive to type I and type II interferon (IFN). In this study, we demonstrate that even in the absence of IFN responses in AG129 (IFN-αβγR(-/-)) mice, Δvhs remains highly attenuated via corneal infection but is fully virulent via intracranial infection. The data demonstrate that the interferon-independent inherent replication defect of Δvhs has a significant impact upon peripheral replication and neuroinvasion.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Bone Marrow Cells / virology
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Cornea / pathology
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Cornea / virology*
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Dendritic Cells / virology
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Herpesvirus 1, Human / pathogenicity*
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Herpesvirus 1, Human / physiology
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Interferon Type I / immunology*
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Interferon-gamma / immunology*
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Keratitis, Herpetic / virology*
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Mice
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Mice, Transgenic
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Ribonucleases / genetics
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Ribonucleases / metabolism*
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Viral Proteins / genetics
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Viral Proteins / metabolism*
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Virus Replication
Substances
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Interferon Type I
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Viral Proteins
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virion host shutoff protein, Simplexvirus
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Interferon-gamma
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Ribonucleases