Key result
Sendai virus causes fatal respiratory lesions in SCID-beige mice lacking natural genetic resistance.
Why the study?
Genetic differences in susceptibility to Sendai virus infection in immunocompetent mice are known, but it is unclear if these differences persist in genetically immunodeficient SCID-beige mice.
Population
Genetically immunodeficient SCID-beige mice of C.B-17 and C57BL/6 strains
Comparison
C.B-17 SCID-beige mice vs C57BL/6 SCID-beige mice
Design
Experimental infection study in genetically distinct SCID-beige mouse strains
Follow-up
Up to 14 to 17 days post-inoculation
Authors
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Alerts to heightened Sendai susceptibility in scid/beige mice; leaves open broader applicability to other models or pathogens.
The genetic differences in susceptibility to Sendai virus infection observed in immunocompetent mice are eliminated by the introduction of scid and beige mutations.
Percy et al. (1994) studied Sendai virus infection. Sendai virus isolate 771076 inoculation vs. C.B-17 SCID-beige mice (compared to C57BL/6 SCID-beige mice) was evaluated on Susceptibility to Sendai virus infection and resulting lesions. Sendai virus infection caused fatal respiratory lesions in both C57BL/6 and C.B-17 SCID-beige mice, demonstrating that scid and beige mutations eliminate natural genetic resistance to the virus.
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