Cellular events in zoster vesicles: relation to clinical course and immune parameters.
The cellular responses in zoster vesicles was studied chronologically in 30 patients, some of whom were compromised hosts with disseminated disease. Cell counts were low initially but rose abuptly later. Polymorphonuclear leukocytes predominated at all times in the vesicular fluid and in the cells adherent to the vesicle base. The abrupt rise in the number of cells generally coincided with an abrupt rise in the titer of vesicular interferon; both increases preceded resolution of local infection and cessation of cutaneous dissemination in disseminated disease, but the sequence of the increases was variable. The peak interferon titer correlated with cessation of dissemination better than did peak cell counts, and the timing of the local events contrasted with appearance of complement-fixing antibody, which commonly occurred after the resolution of disease. Possible interpretations are that a few sensitized lymphocytes may initiate the defensive response, produce interferon, and/or produce chemotactic factors that augment the polymorphonuclear response. The appearance of polymorphonuclear cells may be a nonspecific inflammatory response, or these cells or the deeper mononuclear infiltrate seen in biopsies may contribute to the rise in local interferon.
D000914:Antibodies, Viral; D000917:Antibody Formation; D001706:Biopsy; D003168:Complement Fixation Tests; D006562:Herpes Zoster / Q000276:immunology*; D014645:Herpesvirus 3, Human / Q000276:immunology*; D007372:Interferons / Q000096:biosynthesis*; D007958:Leukocyte Count; D008196:Lymph / Q000276:immunology; D008214:Lymphocytes; D008264:Macrophages; D009000:Monocytes; D009504:Neutrophils
D000914:Antibodies, Viral; D007372:Interferons