Rapid effector function of varicella-zoster virus glycoprotein I-specific CD4+ T cells many decades after primary infection.
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.
Malavige
Gathsaurie Neelika
GN
Medical Research Council Human Immunology Unit, Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, United Kingdom.
Jones
Louise
L
Black
Antony Paul
AP
Ogg
Graham Stuart
GS
D000328:Adult; D015496:CD4-Positive T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism*; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D002478:Cells, Cultured; D002644:Chickenpox / Q000276:immunology*; D014645:Herpesvirus 3, Human / Q000276:immunology* / Q000378:metabolism; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D014759:Viral Envelope Proteins / Q000378:metabolism / Q000494:pharmacology*
D014759:Viral Envelope Proteins; C056913:glycoprotein E, varicella-zoster virus; D007371:Interferon-gamma