. "Appendix J: Prospects for Immunizing Against Herpesvirus varicellae." New Vaccine Development: Establishing Priorities: Volume I, Diseases of Importance in the United States. Washington, DC: The National Academies Press, 1985.
The following HTML text is provided to enhance online
readability. Many aspects of typography translate only awkwardly to HTML.
Please use the page image
as the authoritative form to ensure accuracy.
New Vaccine Development Establishing Priorities, Volume I: Diseases of Importance in the United States
dermatome(s) supplied by the involved ganglion. Generalized dissemination, involvement of motor neurons, and meningoencephalitis also may complicate typical herpes zoster (Weller, 1982).
The varicella-zoster virus has been described often: although certain genetic differences have been identified among strains, the differences evidently do not involve alteration of the relevant antigens that induce protection. Techniques for in vitro culture of this virus and vaccine production also have been described fully elsewhere (Weller, 1982, 1983a).
Host Immune Response
The host immune response following natural varicella involves IgG, IgM, and IgA antibodies (Weller, 1983a). They appear several days after onset of the rash, reach maximum titer during the second or third week after the illness, and decline thereafter. IgA and IgM disappear, usually within a year, but IgG persists at low levels. Humoral antibody levels probably are boosted from time to time by asymptomatic contact with the wild virus (the “streetcar” booster).
The role of humoral antibody in maintaining “latency” is not clear, but following the appearance of herpes zoster, there is a sharp rise in levels of IgG, IgM, and IgA (Weller, 1983a). The cellular immune response is even less well understood. Lymphocytes from otherwise healthly elderly people who develop herpes zoster show little blastogenic response to the viral antigen until several days after the appearance of zoster; specific responses then occur. It appears, therefore, that a depressed cellular immune state is a major factor in the end of latency “containment,” and the pathogenesis of herpes zoster (Weller, 1983a).
Host immune responses to live attenuated varicella vaccine generally mimic those of the natural infection, although the duration of protection is not yet clear. Of even greater concern, however, is the nature of the latent state and the incidence of herpes zoster related to the use of live attenuated varicella-zoster vaccine. Experience with immunization of susceptible immunodeficient children is limited. Several vaccinated leukemic children in Japan have developed zoster (Asano et al., 1983), but there is no evidence that varicella vaccine causes an increase in the frequency or severity of zoster in immunodeficient recipients. The frequency and severity of zoster in normal recipients given varicella vaccine can be assessed only by long-term studies in vaccinated and naturally infected populations (McIntosh, 1984).