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.
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