Attenuation of a field Sendai virus isolate through egg-passages is associated with an impediment of viral genome replication in mouse respiratory cells

@article{Kiyotani2001AttenuationOA,
  title={Attenuation of a field Sendai virus isolate through egg-passages is associated with an impediment of viral genome replication in mouse respiratory cells},
  author={Katsuhiro Kiyotani and Takemasa Sakaguchi and Yutaka Fujii and T. Yoshida},
  journal={Archives of Virology},
  year={2001},
  volume={146},
  pages={893-908}
}
Summary. We investigated the mechanisms responsible for attenuation of mouse pathogenicity of Sendai virus (SeV) through passages in eggs. A highly virulent clone, E0, derived from the field SeV Hamamatsu strain, was successively passaged in hen‘s eggs. Analysis of the mouse lethal dose 50% (MLD50) of virus clones obtained from the viruses at egg-passages 1, 15, 30 and 50 demonstrated that attenuation of E0 by egg-passage occurred due to the gradual appearance of and replacement by virus… 
Identification of Mutations Associated with Attenuation of Virulence of a Field Sendai Virus Isolate by Egg Passage
TLDR
To determine the molecular basis for the attenuation of SeV pathogenicity by egg passage, entire genomes of representative SeV clones isolated during egg passages were sequenced and the significance of the mutations detected in the leader as well as in the L and HN genes was discussed.
Involvement of the Leader Sequence in Sendai Virus Pathogenesis Revealed by Recovery of a Pathogenic Field Isolate from cDNA
TLDR
Recovery of live viruses from cDNA derived from the Hamamatsu strain suggest that leader mutations of SeV affect virus pathogenesis by altering virus replication in a host-dependent manner.
Masking of the contribution of V protein to Sendai virus pathogenesis in an infection model with a highly virulent field isolate.
TLDR
The V protein seems to be potentially functional in the highly virulent Hamamatsu strain and to be prominent if virus replication is restricted, although it appears that the V protein is nonsense in a field isolate of Sendai virus.
Passage of a Sendai Virus Recombinant in Embryonated Chicken Eggs Leads to Markedly Rapid Accumulation of U-to-C Transitions in a Limited Region of the Viral Genome
TLDR
The results suggest that a lack of C proteins could lead unexpectedly to strong selective pressures, and that the C proteins might play more critical roles in SeV replication than ever reported.
Contribution of the leader sequence to homologous viral interference among Sendai virus strains.
TLDR
Results indicate that homologous interference is partly dependent on the promoter sequence and suggest involvement of promoter activity for genome amplification related to host factors in viral interference, and suggest suppression of closely related human paramyxoviruses.
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Its ability to efficiently replicate in nonhuman primates suggests that MPIV1 lacks a significant host range restriction in primates and could theoretically cause zoonotic disease in humans.
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The diet of animal model reflected two extremes of diets which exist in the global population, malnutrition and obesity, and revealed the role of viral mutant spectra dynamics and host immunocompetence in the development of pathogenicity during in vivo passage.
Illumination of Parainfluenza Virus Infection and Transmission in Living Animals Reveals a Tissue-Specific Dichotomy
TLDR
A dichotomy between PIV infection in the URT and trachea versus the lungs is revealed and a new model for studies of pathogenesis, development of live virus vaccines, and testing of antiviral therapies is defined.
Inhibition of Interferon Regulatory Factor 3 Activation by Paramyxovirus V Protein
TLDR
It is shown that the V protein appeared to inhibit translocation of IRF3 into the nucleus, and inhibition by these proteins correlated with interaction of each V protein with IRF 3, indicating that IRf3 is important as an alternative target of paramyxovirus V proteins.
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