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Switch from translation to RNA replication in a positive-stranded RNA virus
1Department of Microbiology and Immunology, University of California, San Francisco, California 94143-0414 USA.
Genes & Development
|August 8, 1998
Summary
Poliovirus genomic RNA translation and replication are controlled by a 5' RNA structure. Cellular factor PCBP up-regulates translation, while viral protein 3CD represses translation and initiates RNA replication.
Area of Science:
- Virology
- Molecular Biology
- Genomics
Background:
- Positive-stranded RNA viruses utilize their genomic RNA for both protein translation and replication.
- The interplay between translation and replication is crucial for viral life cycles but remains incompletely understood.
Purpose of the Study:
- To investigate the interaction between translation and RNA replication processes in positive-stranded RNA viruses.
- To identify regulatory mechanisms controlling the dual use of viral genomic RNA.
Main Methods:
- Poliovirus was used as a model system.
- Analysis of RNA structures at the 5' end of the viral genome.
- Investigated interactions with cellular factor PCBP and viral protein 3CD.
Main Results:
- Viral RNA polymerase cannot replicate RNA templates undergoing translation.
- A specific 5' RNA structure, adjacent to the internal ribosomal entry site, contains regulatory signals.
- PCBP binding enhances viral translation, while 3CD binding represses translation and promotes negative-strand RNA synthesis.
Conclusions:
- The 5' RNA structure acts as a critical regulatory hub for poliovirus.
- Viral protein 3CD binding to this structure dictates whether the genome is used for translation or replication.
- This mechanism provides a switch to control viral gene expression and propagation.