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Genetic dependence of susceptibility to primary infection with Schistosoma mansoni was studied in inbred strains of mice. Eight weeks after the subcutaneous injection of 30 cercariae, C3H/HeJ (H-2k), DBA/1J (H-2q) and BALB/cJ (H-2d) had the highest number of adult worms per animal (8.0-9.8); DBA/2J (H-2d) and 129/J (H-2b) had an intermediate number (6.2-6.4); C57BL/6J (H-2b), BUB/BnJ (H-2q) and CBA/CaJ (H-2k) had the lowest number (3.4-4.0). Studies in congenic mice further suggested that genes within the major histocompatibility complex do not have a major influence on determining the ability of schistosomes to develop into mature adult worms. Results of experiments in which adult worm loads in the F1 generation of C57BL/6J X BALB/cJ were compared with F1 X C57BL/6J and F1 X BALB/cJ backcrosses are consistent with homozygosity for a polygenic phenomenon controlling susceptibility to primary S. mansoni infection. Strain associated differences in parasite development appeared to be related to host defense processes directed against maturing adult worms.
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Fanning et al. (1984) studied this question.
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