Lymphocyte-derived chemotactic factor synthesis in initial genital herpesvirus infection: correlation with lymphocyte transformation

Abstract

Lymphocyte transformation and production of lymphocyte-derived chemotactic factor in response to herpes simplex virus antigen were studied in 15 patients with initial genital herpes and 10 controls. The patients underwent frequent genital examinations, viral cultures, and weekly immunological studies for a period of 11 weeks. The production of lymphocyte-derived chemotactic factor was maximal in week 1 of the disease and declined to control levels by week 6. In contrast, lymphocyte transformation was lowest in week 1, reached a maximum by week 4, and declined to control levels by week 11. Production of lymphocyte-derived chemotactic factor in week 1 was significantly lower in nine patients who developed signs or symptoms of systemic herpes infection than in six who had localized disease. In addition, a marked but transient decline in the production of this lymphokine was observed in patients at the time of clinical recurrence. Virus-specific lymphocyte transformation correlated inversely with the duration of genital pain and lesions and did not correlate with the presence of systemic signs or symptoms. These findings indicate that during initial genital herpes infection the dynamics of lymphocyte transformation and those of lymphocyte-derived chemotactic factor production are different, and that the generation of this lymphokine is an early component of the cellular immune response in this disease. Furthermore, adequate produce of lymphocyte-derived chemotactic factor may be important in restricting herpes simplex virus to the genital area and preventing disease recurrence.

Interferon-λ in immunocompetent individuals with a history of recurrent herpes labialis

“…Given the increased prevalence of HSV-1 infection in the general population, what remains unclear is how susceptibility to HSV recurrences originate only in a small proportion of infected people. Many reports indicate an altered immune response as a correlate of HSV-1 recurrent infection [9][10][11][12][13][14][15][16][17]. A T-helper 1 (Th1)like cytokine response (IFN-γ and IL-2 production) has been associated with resistance to naturally occurring episodes of HL and a T-helper 2 (Th2) profile with a higher susceptibility to recurrent disease [17].…”

“…The number of outbreaks varies widely, ranging from rare episodes to monthly or even more frequent recurrences. The biological basis for the difference between infected individuals who do and those who do not suffer recurrences has long been a subject of clinical and laboratory investigation, including studies of genetic markers [1], epidermal cell susceptibility [4], relative potency of different HSV-1 strains [5,6] and multiple assays of immunological function [1,[7][8][9][10][11][12][13][14][15][16][17].…”