Immunity to herpes simplex virus type 2. V. Risk of recurrent disease following primary infection: modulation of T-cell subsets and lymphokine (LIF) production.

Phenotypic and functional characteristics of peripheral blood lymphocytes (PBL) from 133 patients (87 female; 46 male) with documented primary or recurrent genital HSV-2 infection were determined by serologic testing and CMI [lymphocyte blastogenesis and lymphokine (LF)] evaluation. Primary infection was followed by the development of virus-specific immune memory as defined in vitro by lymphocyte blastogenesis and the development of neutralizing antibody. Virus-specific LIF production was detected by day 5 following primary infection and continued through convalescence. Unlike blastogenesis. LIF response was no longer detected at greater than or equal to 30 days after onset in patients who subsequently developed recurrent disease. It was also suppressed during recrudescence. During convalescence, LIF production returned to levels similar to those for seropositive controls. Patients who did not develop recurrent disease following primary HSV-2 genital infection were LIF positive at greater than or equal to 30 days. The suppression of LIF production during recrudescence and at prodrome correlated with a significant increase in the proportion of OKT8+ and OKIa+ cells. During convalescence (4-9 days after lesion onset), the proportion of OKT8+ and OKIa+ cells returned to normal, remaining constant during the quiescent period (greater than or equal to 14 days). Similar fluctuations were not observed in seropositive controls. Suppression of the LIF response during recrudescence was abrogated by depletion of glass-adherent OKIa+ and OKT8+ cells or by complement-mediated cytolysis using OKT8, OKM2, or OKIa antibody. PBL obtained from patients during primary genital HSV-2 infection exhibited an increase in the OKT10+ and OKM2+ cells.