Genetics of natural resistance to Sendai virus infection in mice.
The genetics of resistance to a naturally occurring respiratory infection caused by Sendai virus was examined in F1, F2, and backcross progeny of resistant C57BL/6J and susceptible DBA/2J mice and in 25 recombinant inbred strains. An intranasal inoculum of 0.1 50% tissue culture infective dose (low dose) of Sendai virus caused 0% mortality in C57BL/6J and F1 mice and 73% mortality in DBA/2J mice. An inoculum of 1.0 50% tissue culture infective dose (high dose) caused 3, 0, and 89% mortality in C57BL/6J, F1, and DBA/2J mice, respectively. Low-dose infection caused 36% mortality in F1 X DBA/2J hybrids and 0% mortality in F2 hybrids. High-dose infection caused 29 and 32% mortality in F1 X DBA/2J and F2 hybrids, respectively. Resistance was not linked to H-2 haplotype, coat color, or sex. High-dose infection caused deaths in 12 recombinant inbred strains, and the strain distribution pattern was concordant with that of a chromosome 1 marker, Sas-1, in 20 of 25 strains (P less than 0.01). Resistance therefore behaved as a simple Mendelian dominant trait which presumptively mapped to chromosome 1.
D000818:Animals; D002874:Chromosome Mapping; D003433:Crosses, Genetic; D005799:Genes, Dominant; D008040:Genetic Linkage; D006183:H-2 Antigens / Q000235:genetics; D007113:Immunity, Innate; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D010222:Parainfluenza Virus 1, Human; D018184:Paramyxoviridae Infections / Q000235:genetics / Q000276:immunology*
D006183:H-2 Antigens