. "Appendix D-11: The Prospects for Immunizing Against Rabies Virus." New Vaccine Development: Establishing Priorities: Volume II, Diseases of Importance in Developing Countries. Washington, DC: The National Academies Press, 1986.
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New Vaccine Development: Establishing Priorities, Volume II, Diseases of Importance in Developing Countries
leading to the production of large numbers of viral particles in the salivary glands. This replication may occur before clinical symptoms appear, facilitating transmission through the saliva. In addition, some animals may become viral secretors, spreading disease over long periods of time without developing the disease.
Humans are nontransmitting hosts for rabies virus. There are no documented cases of human-to-human spread of rabies, other than several cases resulting from corneal transplantation from unrecognized rabies victims.
HOST IMMUNE RESPONSE
Infection with rabies virus induces a humoral immune response, which in humans is not sufficient to prevent disease and death. Antirabies antibodies can prevent disease, however, if given passively before or shortly after infection. Possible explanations for this situation are that the humoral immune response is not rapid enough after infection, that a disrupted cell-mediated immune response (CMI) interferes with eradication of the virus, or that the intraneural infection is protected from the antibody response.
Rabies virus does cause immunosuppression of the CMI response through enhancement of suppressor T-cell action. A state of anergy develops in which cytotoxic T-cells fail to act against rabies and other antigens.
It also appears that low levels of protective antibody, resulting either from a suboptimal or decayed vaccination response, or from inadequate passive immunization, can lead to paradoxical immunosuppression and accelerated disease (Shope, 1984). The possibility of such an occurrence dictates that any new vaccine must be strongly immunogenic and that the duration of protective immunity be predictable.
Rabies infection also induces interferon production, which may provide some protection by slowing the progress of disease. It is not yet known if the interferon response could be utilized therapeutically in early post-exposure prophylaxis or treatment.
Finally, incomplete viral particles, called T particles (Shope, 1984), may be present in the infective inoculum or produced during the early course of disease. These particles cannot cause disease, but may interfere with the early course of infection by competing for cell membrane receptor sites, for example. The effect of T particles on the development of the immune response is not clear, although they may prolong the incubation period and allow more time for post-exposure prophylaxis.
DISTRIBUTION OF DISEASE
Canine rabies is enzootic in at least 87 countries and on every continent except Australia. Such islands as Hawaii, New Zealand, and