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Genetic‐linked variation in susceptibility of mice to Schistosomiasis mansoni
Author(s) -
FANNING MARY M.,
KAZURA J.W.
Publication year - 1984
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1984.tb00784.x
Subject(s) - congenic , schistosoma mansoni , biology , schistosomiasis , inbred strain , genetics , major histocompatibility complex , immunology , helminths , gene , strain (injury) , parasite hosting , anatomy , computer science , world wide web
Summary 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‐2 k ), DBA/1J (H‐2 q ) and BALB/cJ (H‐2 d ) had the highest number of adult worms per animal (8–0–9–8); DBA/2J (H‐2 d ) and 129/J (H‐2 b ) had an intermediate number (6–2–6–4); C57BL/6J (H‐2 b ), BUB/BnJ (H‐2 q ) and CBA/CaJ (H‐2 k ) 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 F| generation of C57BL/6J x BALB/cJ were compared with F, x C57BL/6J and F, 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.