Document 0783 DOCN M9650783 TI Th1/Th2-like immunity and resistance to herpes simplex labialis. DT 9605 AU Spruance SL; Evans TG; McKeough MB; Thai L; Araneo BA; Daynes RA; Mishkin EM; Abramovitz AS; Department of Medicine, University of Utah, Salt Lake City 84132,; USA. SO Antiviral Res. 1995 Sep;28(1):39-55. Unique Identifier : AIDSLINE MED/96105496 AB To investigate potential immunologic mechanisms of resistance to recurrent herpes simplex labialis, we assayed serum antibody titers and cultured peripheral blood mononuclear cell (PBMC) cytokine production among patients with a history of frequent episodes (H+S+), herpes simplex virus (HSV)-seropositive individuals without a history of herpes labialis (H-S+) and HSV-seronegative persons (H-S-). In addition, H+S+ patients were exposed to experimental ultraviolet radiation (UVR) on the lips and the immunologic assay results compared among those who developed experimental lesions and those who did not. H+S+ patients were found to have higher median serum titers of HSV antibody and trends to lower levels of HSV-specific PBMC IFN-gamma and IL-2 than H-S+ control patients (123 vs 66, P = 0.04; 424 vs 548 pg/ml, P = 0.08; 14 vs 26 pg/ml, P = 0.14, respectively). Correlation of the results with the occurrence of experimental lesions showed the inverse: the subgroup of H+S+ patients with UVR-induced lesions had lower titers of antibody and trends to higher levels of IFN-gamma and IL-2 than H+S+ patients who could not be induced (93 vs 149, P = 0.02; 501 vs 347 pg/ml, P = NS; 26 vs 11 pg/ml, P = NS, respectively). The size and duration of UVR-induced lesions showed positive correlations with IFN-gamma and IL-2 levels (r = 0.60-0.67, P = 0.02-0.04). Although the small number of patients limited the power of this study, the overall pattern of the findings suggests that a Th1-like cytokine response (IFN-gamma and IL-2 production) may be associated with resistance to naturally occurring episodes of herpes labialis. The development and severity of experimental UVR-induced herpes labialis appears to be regulated differently and may involve an immunopathologic mechanism. DE Antibodies, Viral/BLOOD Cells, Cultured Cytokines/*IMMUNOLOGY Herpes Labialis/*IMMUNOLOGY Human Immunity, Natural Leukocytes, Mononuclear/IMMUNOLOGY Lip Diseases/VIROLOGY Recurrence Support, Non-U.S. Gov't Support, U.S. Gov't, P.H.S. Th1 Cells/*IMMUNOLOGY Th2 Cells/*IMMUNOLOGY Ultraviolet Rays JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).