Immunity to herpes simplex virus type 2. IV. Impaired lymphokine production during recrudescence correlates with an imbalance in T lymphocyte subsets.
Cell-mediated immunity (CMI) to herpes simplex virus type 2 (HSV-2) was studied in patients with recurrent disease. Peripheral blood lymphocytes (PBL) obtained during recrudescence (0 to 3 days post-onset of lesion), convalescence (4 to 14 days), and quiescence (greater than 14 days), which were cultured in vitro in the presence of UV-inactivated HSV-2 (G) antigen, demonstrated similar, virus-specific lymphoproliferative responses. However, the production of the lymphokine, leukocyte migration-inhibition factor (LIF), was completely suppressed during recrudescence. During convalescence, LIF production returned to levels similar to those of PBL from seropositive controls (without a history of recurrent subsets revealed a significant increase in the proportion of T8+ and Ia+ cells during recrudescence and at prodrome (24 to 48 hr before onset of lesions). Glass adherence reduced the proportion of both T8+ and Ia+ cells and restored early (1 day) LIF activity, and recrudescent PBL suppressed the proliferation of autologous T cells in presence of UV-HSV-2 (G) antigen. The expression of both phenotypes and LIF production returned to control levels during convalescence.
D000911:Antibodies, Monoclonal / Q000276:immunology; D006561:Herpes Simplex / Q000276:immunology*; D000949:Histocompatibility Antigens Class II / Q000276:immunology; D006801:Humans; D007111:Immunity, Cellular; D007961:Leukocyte Migration-Inhibitory Factors / Q000096:biosynthesis; D008213:Lymphocyte Activation; D008222:Lymphokines / Q000096:biosynthesis*; D012008:Recurrence; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology*
D000911:Antibodies, Monoclonal; D000949:Histocompatibility Antigens Class II; D007961:Leukocyte Migration-Inhibitory Factors; D008222:Lymphokines