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Origin and evolution of the c-src-transducing avian sarcoma virus PR2257
B A Yatsula1, J Geryk, J Briestanska
1Unité de Recherche Associée 1443 du Centre National de la Recherche Scientifique, Institut Curie, Orsay, France.
The Journal of General Virology
|October 1, 1994
Summary
Avian sarcoma virus PR2257 evolved into PR2257/16 after in vivo passages, showing increased viral titer. This evolution involved recombination with a helper virus, not endogenous virus sequences, challenging prior hypotheses.
Area of Science:
- Virology
- Molecular Biology
- Oncology
Background:
- Avian sarcoma virus PR2257 transduces the c-src gene and associated sequences.
- The initial PR2257 isolate contained endogenous virus (ev) sequences, suggesting recombination.
- The role of endogenous viruses in c-src transduction remained unclear.
Purpose of the Study:
- To investigate the evolution of avian sarcoma virus PR2257 during in vivo passaging.
- To determine the genetic changes in the highly infectious PR2257/16 variant.
- To clarify the involvement of endogenous virus sequences in c-src transduction.
Main Methods:
- In vivo passaging of the original tumor.
- Viral titration to quantify infectious particles.
- Whole-genome sequencing of PR2257 and PR2257/16.
- Analysis of proviral DNA from tumor samples.
Main Results:
- Repeated in vivo passaging led to a tenfold increase in viral titer, yielding PR2257/16.
- PR2257/16 resulted from recombination between PR2257 and the env gene of a helper virus, with five point mutations.
- Early tumor passages lacked endogenous virus sequences, unlike the C7 cell line isolate.
Conclusions:
- The evolution of PR2257 to PR2257/16 involved helper virus recombination and point mutations, not endogenous virus involvement.
- The presence of ev sequences in the C7 cell line isolate was likely an artifact of cell culture or early passage manipulation.
- These findings do not support the hypothesis that endogenous virus sequences mediate c-src transduction.