Characterization of a new isolate of poliovirus defective interfering particles

@article{Lundquist1979CharacterizationOA,
  title={Characterization of a new isolate of poliovirus defective interfering particles},
  author={R E Lundquist and Margery A. Sullivan and Jacob V. Maizel},
  journal={Cell},
  year={1979},
  volume={18},
  pages={759-769}
}
Infectious cDNA Clone
TLDR
This work constructed several well-defined mutations in the nonstructural portion of the poliovirus type I (Mahoney strain) genome by making small insertions in an infectious cDNA clone, providing the first unambiguous evidence that the non structures of thePoliovirus genome contains multiple complementation groups.
In vitro construction of poliovirus defective interfering particles
TLDR
Observations indicate that deletion RNAs that are inactive replicons have little or no possibility of being genomes of DI particles suggesting the existence of a nonstructural protein(s) that has an inclination to function as a cis-actingprotein(s).
Experimental and mathematical insights on the competition between poliovirus and a defective interfering genome
TLDR
An ordinary differential equation model is developed to infer the effect of the interaction between defective interfering (DI) replicons and wild-type (WT) poliovirus and finds that DI replicates faster than WT, but an equilibrium is established when both WT and DI compete for resources needed for RNA replication and genome encapsidation.
Guanidine-resistant defective interfering particles of poliovirus
TLDR
A mixture containing standard poliovirus and D3 particles (mutants with deletions in the capsid locus) was serially passaged in the presence of guanidine and produced two novel proteins, which had molecular weights of approximately 68,000 and 25,000.
Encapsidation studies of poliovirus subgenomic replicons.
TLDR
Results suggest that a specific encapsidation process operates and that it does not involve RNA sequences within the region of the genome encoding the capsid proteins.
Persistent Enterovirus Infection: Little Deletions, Long Infections
TLDR
How the TD genomes arise, how they interact with the host, and their effects on host biology are discussed are discussed.
Complementation of a poliovirus defective genome by a recombinant vaccinia virus which provides poliovirus P1 capsid precursor in trans
TLDR
This is the first report of the generation of a pure population of defective polioviruses free of contaminating wild-type poliovirus.
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References

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Defective Interfering Particles of Poliovirus IV. Mechanisms of Enrichment
TLDR
Study of the cycloheximide effect showed that the drug acted as if to change the input ratio of standard to DI particles, and enrichment due to preferential encapsidation of DI RNA can be explained as aspects of two different phenomena.
Defective Interfering Particles of Poliovirus I. Isolation and Physical Properties
TLDR
A class of defective interfering (DI) poliovirus particles has been identified and competition hybridization experiments indicate that DI RNA is 80 to 90% of the length of standard RNA.
The isolation of simian virus 40 variants with specifically altered genomes.
Serial passage of simian virus 40 (SV40) at high multiplicity of infection leads to the emergence of variants with deleted, substituted, and/or duplicated DNA. Individual variants have been cloned by
Capsid protein precursor is one of two initiated products of translation of poliovirus RNA in vitro
Previous studies in our laboratory have demonstrated that cell-free systems translating the Mahoney strain of poliovirus type I RNA utilize two unique initiation sites. In this study,
Virus-specified protease in poliovirus-infected HeLa cells.
TLDR
The conclusion is that a non-structural poliovirus gene product participates in protein cleavages that produce the viral coat proteins.
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