Related Experiment Videos
Genetics of natural resistance to Sendai virus infection in mice
Abstract:
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.
Insights
Genetic resistance to Sendai virus respiratory infection in mice is a simple Mendelian dominant trait. This resistance is linked to a marker on chromosome 1, suggesting a specific genetic locus controls this immune response.
Area of Science:
- Immunogenetics
- Virology
- Mouse Models of Disease
Background:
- Sendai virus is a common respiratory pathogen causing significant mortality in susceptible mouse strains.
- Understanding the genetic basis of resistance is crucial for developing effective disease control strategies.
- Previous studies have not fully elucidated the genetic factors governing resistance to Sendai virus.
Purpose of the Study:
- To investigate the genetic control of resistance to Sendai virus-induced respiratory infection in mice.
- To identify the chromosomal location of genes influencing Sendai virus resistance.
Main Methods:
- Crossbreeding experiments involving resistant (C57BL/6J) and susceptible (DBA/2J) mouse strains (F1, F2, backcross progeny).
- Infection of mice with varying doses of Sendai virus (0.1 and 1.0 50% tissue culture infective dose).
- Analysis of mortality rates and linkage analysis with known genetic markers in 25 recombinant inbred strains.
Main Results:
- Mortality varied significantly between resistant and susceptible strains, with intermediate rates in hybrids.
- Resistance to Sendai virus was not associated with H-2 haplotype, coat color, or sex.
- Linkage analysis in recombinant inbred strains indicated that resistance is concordant with a chromosome 1 marker (Sas-1), suggesting localization to this chromosome.
Conclusions:
- Resistance to Sendai virus behaves as a simple Mendelian dominant trait.
- The primary gene(s) conferring resistance to Sendai virus are located on mouse chromosome 1.
- These findings provide a foundation for further molecular mapping and characterization of the genetic basis of Sendai virus resistance.