Key result
The VdeltaC mutant virus, lacking the C-terminal half of the V protein, displayed normal in vitro phenotypes but attenuated in vivo pathogenicity in mice, mapping the pathogenicity determinant to the C-terminal half.
Population
Mice and in vitro cells
Comparison
VdeltaC mutant Sendai virus vs V(-) mutant virus and wild-type Sendai virus
Design
Preclinical
Authors
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Identifies a Sendai virus pathogenicity determinant in mice; leaves open relevance to human disease or interventions.
The cysteine-rich C-terminal half of the Sendai virus V protein is the primary determinant for in vivo viral pathogenesis.
Kato et al. (1997) studied Sendai virus infection. VdeltaC mutant virus vs. V(-) mutant and wild-type viruses was evaluated on In vitro and in vivo phenotypes (gene expression, cytopathogenicity, and pathogenicity in mice). The VdeltaC mutant virus, lacking the C-terminal half of the V protein, displayed normal in vitro phenotypes but attenuated in vivo pathogenicity in mice, mapping the pathogenicity determinant to the C-terminal half.
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