Rapid Effector Function of Varicella-Zoster Virus Glycoprotein I-Specific CD4+ T Cells Many Decades after Primary Infection
Identifieur interne : 002B89 ( Main/Exploration ); précédent : 002B88; suivant : 002B90Rapid Effector Function of Varicella-Zoster Virus Glycoprotein I-Specific CD4+ T Cells Many Decades after Primary Infection
Auteurs : Gathsaurie Neelika Malavige [Royaume-Uni, Sri Lanka] ; Louise Jones [Royaume-Uni] ; Antony Paul Black [Royaume-Uni] ; Graham Stuart Ogg [Royaume-Uni]Source :
- The Journal of Infectious Diseases [ 0022-1899 ] ; 2007.
Abstract
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-γ 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 gIspecific CD4+ T cell involvement in the control of VZV replication.
Url:
DOI: 10.1086/511274
Affiliations:
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<front><div type="abstract">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-γ 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 gIspecific CD4+ T cell involvement in the control of VZV replication.</div>
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