Interferon, antibody, and other host factors in herpes zoster

Abstract

A B S T R A C T 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 phytohernagglutinin 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.

Pathogenesis of Rift Valley fever in rhesus monkeys: role of interferon response

“…Studies have shown that in some diseases an early interferon response can be predictive of the outcome. A correlation between levels of vesicle interferon and the course of disease was shown in herpes zoster infection [25]. Patients could be separated based on the later rise of vesicle interferon in those with disseminated disease.…”

Selective Increase in Lymphocyte Interferon Response to Vaccinia Antigen after Revaccination

“…Also, enhanced local interferon production by immunized mice has been observed after intracranial challenge with vaccinia (26). That such local interferon may play a very important role in recovery or resistance to reinfection has been documented by studies of Varicella zoster (another enveloped DNA virus affecting the skin) in patients with impaired cell-mediated immunity (27). It was shown, in such patients, that a delay in appearance of interferon at the local site was associated with severe progressive infections and that the appearance of high local titers of interferon signaled the onset of recovery.…”

Evaluation of Topical Polyinosinic Acid-Polycytidylic Acid in Treatment of Localized Herpes Zoster in Children with Cancer: a Randomized, Double-Blind Controlled Study

“…Our study evaluated the clinical effects of topical poly(I:C) at a time during the infectious process when interferon levels in vesicle fluid could be expected to be minimal (1,19). Although concentrations of interferon in vesicle fluid were not measured in our children, we can postulate possible mechanisms for the lack of therapeutic efficacy of the drug.…”

“…The cutaneous lesions of this infection are clearly visible, so that the course of the disease can be followed without difficulty. Interferon reaches its maximum concentration in vesicle fluid just before the lesions stop progressing, while circulating levels of the glycoprotein remain low (1,19). The sensitivity of varicella-zoster virus to interferon has already been established in vitro (2).…”