Abstract
The challenge virus standard-11 strain (CVS) of fixed rabies virus produces neuronal apoptosis in widespread areas of the brain of mice after intracerebral inoculation. The role of the adaptive immune response in producing neuronal apoptosis in this model was evaluated by comparing the infections in adult C57BL/6J mice with nude mice (T cell deficient) and Rag1 mice (T and B cell deficient). Both strains of immunodeficient mice showed very similar clinical disease and neuropathological findings, including marked neuronal apoptosis. The adaptive immune response is unlikely of fundamental importance in producing neuronal apoptosis in the brains of mice in this model.
The authors are grateful for technical assistance from Pamini Rasalingam, statistical advice from Dr. Miu Lam (Department of Community Health and Epidemiology, Queen's University), and for the gift of monoclonal antibody 5DF12 from Dr. Alexander I. Wandeler (Centre for Rabies Expertise, Canadian Food Inspection Agency, Nepean, Ontario). This work was supported by Canadian Institutes of Health Research grant MOP-64376 and the Queen's University Violet E. Powell Research Fund (both to A.C. Jackson).