Journal
IMMUNITY
Volume 18, Issue 5, Pages 593-603Publisher
CELL PRESS
DOI: 10.1016/S1074-7613(03)00112-2
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Funding
- NEI NIH HHS [P30 EY001792-209001, R01 EY005945-13, P30 EY008098, P30 EY008098-11, P30 EY008098-10, P30 EY008098-129003, R01 EY005945-14, P30 EY008098-119003, EY05945, EY07397, R01 EY005945, P30 EY008098-12, P30 EY001792-209002, P30 EY001792, R01 EY005945-15, P30 EY08098] Funding Source: Medline
- NIAID NIH HHS [AI49719, R01 AI049719] Funding Source: Medline
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This study challenges the concept that herpes simplex virus type 1 (HSV-1) latency represents a silent infection that is ignored by the host immune system, and suggests antigen-directed retention of memory CD8(+) T cells. CD8(+) T cells specific for the immunodominant gB(498-505) HSV-1 epitope are selectively retained in the ophthalmic branch of the latently infected trigeminal ganglion, where they acquire and maintain an activation phenotype and the capacity to produce IFN-gamma. Some CD8(+) T cells showed TCR polarization to junctions with neurons. A gB(498-505) peptide-specific CD8(+) T cell clone can block HSV-1 reactivation from latency in ex vivo trigeminal ganglion cultures. We conclude that CD8+ T cells provide active surveillance of HSV-1 gene expression in latently infected sensory neurons.
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