Abstract
Control of ganglionic herpes simplex virus (HSV) infection depends on CD8(+) cells but not on the death of infected neurons. Primarily, perforin and granzyme B mediate CD8(+) cell cytotoxicity, whereas the in vivo functions of granzyme A, a third granule protein, are unknown. Here, it is shown that granzyme A restricts the interneuronal spread of HSV and significantly influences ganglionic virus load.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antiviral Agents / physiology*
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Disease Models, Animal
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Ganglia, Spinal / immunology
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Ganglia, Spinal / pathology
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Ganglia, Spinal / virology
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Granzymes
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Herpes Simplex / immunology*
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Herpes Simplex / pathology
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Herpes Simplex / virology
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Herpesvirus 1, Human / immunology
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Herpesvirus 1, Human / physiology
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Humans
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Peripheral Nervous System / virology*
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Serine Endopeptidases / genetics
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Serine Endopeptidases / physiology*
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T-Lymphocytes, Cytotoxic / immunology*
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Viral Load
Substances
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Antiviral Agents
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Granzymes
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Serine Endopeptidases
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GZMA protein, human