Background. Kaposi's varicelliform eruption (KVE) is characterized by disseminated cutaneous eruptions usually caused by infection with herpes simplex virus (HSV). Kaposi's varicelliform eruption is commonly observed among patients with atopic dermatitis (AD). Why AD patients are prone to HSV infections is still an enigma. Recent findings suggest that an increased number of IL-4-secreting cells can be cloned from lesions of AD. Because IL-4 is a known Th1 cell inhibitor, theoretically, by inhibiting the Th1 cells, it could downregulate the immune response against HSV. In this study, we have evaluated the role of IL-4 on HSV replication. Methods. Peripheral blood mononuclear cells (PBMC) from 10 HSV seronegative and five seropositive healthy individuals were stimulated with PHA, recall antigen (tetanus toxoid), and HSV antigen in combination with IL-4 and anti-IL-4. Supernatants were assessed for interferon (IFN) gamma, IL-4 by enzyme-linked immunosorbent assay (ELISA), and for anti-HSV effect. Anti-HSV effect was assessed by measuring inhibition of the cytopathic effect (CPE) of HSV on a Vero cell line. Results. Both seropositive and seronegative groups showed significant inhibition of lFN-gamma secretion with addition of IL-4 (P < .001, Wilcoxon rank sum test) and this effect could be neutralized by anti-IL-4. There was a direct relationship between the IFN-gamma concentration and the HSV cytopathic effect and an inverse relationship between IL-4 concentration and HSV CPE. Conclusions. This study provides evidence that IL-4 can enhance HSV infection. Therefore, it is conceivable that patients with conditions of increased activity of IL-4, as in AD, would be prone to extensive forms of HSV infection.
|Original language||English (US)|
|Number of pages||3|
|Journal||International Journal of Dermatology|
|State||Published - 1995|
ASJC Scopus subject areas