Interferon, antibody, and other host factors in herpes zoster

David A. Stevens; Thomas C. Merigan

doi:10.1172/JCI106910

Interferon, antibody, and other host factors in herpes zoster

David A. Stevens and Thomas C. Merigan

Published May 1, 1972 - More info

View PDF

Abstract

The influence of several factors on the course of herpes zoster was studied in 151 patients. Dissemination of zoster was associated with the presence of a concurrent disease, especially Hodgkin's disease, and/or the use of immunosuppressive therapy. Several host-immune parameters, including quantitative immunoglobulins, circulating lymphocyte counts, delayed hypersensitivity to multiple skin test antigens, and lymphocyte transformation to phytohemagglutinin did not correlate with dissemination of disease. Development of virus-specific complement-fixing antibody (CFA) was delayed in some patients with disseminated disease.

Vesicle interferon (V-IF) titers were low early in the disease in patients with localized and disseminated zoster and then rose, usually abruptly, to a peak value and declined as pustulation and crusting occurred. However, titers in patients with localized disease rose at an earlier time. This could be seen in terms of time to development of intermediate values of V-IF or by the day on which the sharpest rise occurred. In 15 carefully studied patients with disseminated disease, the development of the maximum V-IF response was followed within 48 hr by cessation of dissemination. Half of the patients in this group had no CFA detectable until after dissemination had ceased.

These findings suggest at least two host factors whose interaction might determine host response to zoster; local interferon production (possibly mediated by sensitized lymphocytes) and humoral antibody, acting to prevent or shorten dissemination of an initially local disease.