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On the model of Syrian hamsters inoculated intracerebrally with 9 tick-borne encephalitis (TBE) virus strains varying in virulence, the specific involvement of the organs of the immune system (spleen and lymph nodes) was established and morphological features of the process described. The most severe destructive changes of these organs were found in the hamsters inoculated with highly virulent strains which appeared to be one of the factors leading to 100% death of the animals. In hamsters inoculated with strains of low virulence, the destructive changes in immunogenesis organs were less marked, but active migration and proliferative processes developed in them.
View Article and Find Full Text PDFMechanism of specific resistance development in experimental tick-borne encephalitis (TBE) and possible effects on this mechanism were studied. Thorough characterization of the immune status of animals included quantitative and functional changes in populations of T and B lymphocytes determined over time via changes in the rosette-forming and antibody producing cells, antihemagglutinins, and index of migration inhibition. Stimulation or inhibition of some links of immunogenesis by means of preparations of directed effect (carageenan, ascorbic acid, heterologous serum, theophylline, levamisole) was reflected in parameters of the immune status and pathogenetic features of TBE.
View Article and Find Full Text PDFInactivated concentrated and unconcentrated vaccines against tick-borne encephalitis given to 80 normal subjects produced no suppressing effect on the quantitative values of the immune status. Immunogenesis was characterized by stimulation of both T- and B-links of the immune system of the vaccines. With the unconcentrated vaccine a greater response was demonstrated after 3 injections; the concentrated vaccine induced an intensive immune response after 2 injections.
View Article and Find Full Text PDFThe literature on tick-borne fever is reviewed. Tick-borne fever is a rickettsial disease of sheep and cattle characterised by high fever and severe leucopaenia. The causative agent, Cytoecetes phagocytophila invades the neutrophils and monocytes and is transmitted by the tick Ixodes ricinus.
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