Abstract
Cellulair immunity to HSV-1 in 10 children and adults with recurrent herpes labialis was evaluated with two microassays: (1) Blastogenesis: lymphocytes were incubated with tissue culture cells (MA-160) persistently infected with HSV-1. Uninfected MA-160 cells were used as controls with a blastogenic index (BI) calculated from cpm of C14 thymidine uptake for lymphocytes incubated with infected cells divided by uptake following incubation with uninfected cells. (2) Cytotoxicity: utilizing the same persistently infected cell line as target cells, release of 51Cr from these cells or controls was used as the index of lymphocyte reactivity (Steele, R. W. et al. J.Immunol. 110:1502, 1973). Blastogenesis for subjects with recurrent herpes labialis demonstrated a mean BI of 25.9(7.8-49). The mean BI in control donors was 17.6(5.3-40). In the cytotoxicity assay specific immune release attributable to HSV-1 averaged 2.8% (0-5.7%) in patients compared to 14.9%(8.0-31.5%) in controls. These data suggest a dissociation between the afferent and efferent mechanisms of cellular immunity with normal or enhanced lymphocyte blastogenesis but decreased cytotoxicity. Recurrent herpes labialis may therefore be a consequence of subtle cellular immune deficiency involving at least one of the efferent mechanisms.
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