In C57BL/6 (B6) mice, most herpes simplex virus (HSV)-specific CD8 T cells recognize a strongly immunodominant epitope on glycoprotein B (gB498) and can inhibit HSV type 1 (HSV-1) reactivation from latency in trigeminal ganglia (TG). To study the antigen specificity of cornea-infiltrating T cells in HSK patients, T cells were isolated and expanded by mitogenic stimulation from corneas of 2 patients with HSV-1-mediated HSK. In this study, the CD4+ T-cell responses against the herpes simplex virus type 2 (HSV-2) tegument protein VP16 were studied in two HSV-2–infected subjects at two different time points that spanned a 5-year period. We show that CD4+ FoxP3+ Tregs up- regulate HVEM (herpes virus entry mediator), which is a binding site for major viral glycoprotein HSVgD, following HSV infection, which is a binding site for major viral glycoprotein HSVgD. Chen, D. Bromodeoxy uridine (BrdU) incorporation measured cell proliferation in vivo.RESULTS: TAK-779 treatment during acute HSV-1 infection reduced the number of infiltrating CD8+ T cells but did not alter the number of viral genome copies. Clearance of infectious virus from neural tissues was not significantly different in perforin-deficient or FasL-defective mice compared to wild-type mice.
Some of these virus proteins use methods that may prevent them from being recognised by the T cells. Thus, HVS transformation is a suitable model for T cell immunodeficiency studies and characterization. Immunization reduced the expression of PD-1, a marker of T-cell exhaustion, in the TG of ocularly challenged mice, and mock-immunized CD8α(-/-) mice had lower levels of PD-1 expression and latency than mock-immunized WT or CD8β(-/-) mice.