Murine malaria: genetic control of resistance to Plasmodium chabaudi.

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Strain variation in the level of resistance to malaria was investigated in inbred strains of mice after infection with Plasmodium chabaudi. When infected intraperitoneally with 10(6) P. chabaudi-parasitized erythrocytes, mice of 11 inbred strains could be separated into two groups by using survival time as the criterion; C57BL/6J, C57L/J, DBA/2J, CBA/J, and B10.A/SgSn mice were found to be resistant to P. chabaudi, whereas A/J, DBA/1J, BALB/c, C3H/HeJ, AKR/J, and SJL/J mice were susceptible. An examination of F1 hybrids revealed that resistance was dominant over susceptibility. A segregation analysis of backcross and F2 progeny derived from susceptible A/J and resistant B10.A/SgSn parental mice suggested that host resistance in this strain combination was genetically controlled by a single, dominant, non-H-2-linked gene. Inheritance of resistance was autosomal, but expression of the trait was influenced by the sex of the host, female mice being more resistant than male mice. Phenotypic expression of the resistance gene was apparent within 6 days of infection as a significant difference between resistant and susceptible mice in the level of parasitemia. A preliminary analysis of the mechanism of resistance showed that compared with susceptible A/J mice, resistant B10.A/SgSn hosts had an augmented erythropoietic response during the course of malaria, as well as phenylhydrazine-induced anemia. These results suggest that the ability to replace destroyed erythrocytes quickly and efficiently may determine host survival after infection with P. chabaudi.

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