Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 195, Issue 5, Pages 660-664Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/511274
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Funding
- Medical Research Council [MC_U137881017, G116/150] Funding Source: Medline
- MRC [G116/150, MC_U137881017] Funding Source: UKRI
- Medical Research Council [MC_U137881017, G116/150] Funding Source: researchfish
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Glycoprotein I ( gI) of varicella-zoster virus ( VZV) contributes to viral virulence and is therefore a potentially important target for T cell control of viral replication. Persisting effector function of gI-specific T cells after primary infection has not been previously examined. We have shown that, many decades after infection, relatively high frequencies gI-specific interferon-gamma responses are detectable ex vivo and are dominated by CD4(+) T cells. We characterized the optimal peptide of the strongest response in our cohort showing restriction through DRB4*01. These findings are consistent with gI-specific CD4(+) T cell involvement in the control of VZV replication.
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