Key Points
- To investigate cell-mediated immunity and regulatory T-lymphocyte dynamics across the clinical phases of recurrent herpes simplex virus type 2 infection.
- Assessed peripheral blood lymphocytes from patients with recurrent HSV-2 across recrudescence (0–3 days post-lesion), convalescence (4–14 days), and quiescence (>14 days), alongside seropositive controls.
- Cultured cells in vitro with UV-inactivated HSV-2 antigen to measure virus-specific lymphoproliferation and leukocyte migration-inhibition factor (LIF) production.
- Phenotyped T-cell subsets and evaluated the effect of glass-adherence cell depletion on suppressor cell activity and LIF restoration.
- Leukocyte migration-inhibition factor production was completely suppressed during recrudescence despite intact lymphoproliferative responses, returning to control levels during convalescence.
- Proportions of T8+ and Ia+ cells increased significantly during recrudescence and the prodromal phase (24 to 48 hours before lesion onset).
- Depleting T8+ and Ia+ cells through glass adherence abolished suppression of autologous T-cell proliferation and restored early LIF activity.
Structured PICO
PPopulationPatients with recurrent herpes simplex virus type 2 (HSV-2) disease and seropositive controls without a history of recurrent disease.
IInterventionIn vitro culture of peripheral blood lymphocytes (PBL) in the presence of UV-inactivated HSV-2 (G) antigen.
CComparatorPBL from seropositive controls without a history of recurrent disease.
OOutcomeProduction of leukocyte migration-inhibition factor (LIF) and lymphoproliferative responses.surrogate
Impaired lymphokine production during HSV-2 recrudescence correlates with an imbalance in T lymphocyte subsets, specifically an increase in T8+ and Ia+ cells.