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Transcription of vesicular stomatitis virus is required to shut off cellular RNA synthesis
Abstract:
RNA synthesis by mouse myeloma (MPC-11) cells was rapidly and progressively shut off by infection with vesicular stomatitis virus temperature-sensitive (ts) mutants permissive for transcription. In sharp contrast, mutants or defective vesicular stomatitis virions restricted in transcription were incapable of causing progressive inhibition of cellular RNA synthesis even at massive multiplicities of infection. A viral product synthesized 30 to 60 min after permissive infection with tsG114(I) appeared to be essential for prolonged inhibition of RNA synthesis in cells switched up to restrictive temperature.
Insights
Vesicular stomatitis virus (VSV) mutants that can transcribe RNA shut down host cell RNA synthesis. A viral product is essential for this prolonged inhibition, highlighting VSV
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Vesicular stomatitis virus (VSV) is a non-segmented negative-strand RNA virus.
- Understanding viral mechanisms that inhibit host cell processes is crucial for virology research.
Purpose of the Study:
- To investigate the role of VSV transcription in the inhibition of host cell RNA synthesis.
- To identify viral factors responsible for the shutdown of cellular RNA production.
Main Methods:
- Infection of mouse myeloma (MPC-11) cells with VSV temperature-sensitive (ts) mutants.
- Analysis of cellular RNA synthesis rates under different infection conditions and temperatures.
- Identification of viral products synthesized post-infection.
Main Results:
- VSV mutants permissive for transcription rapidly inhibited cellular RNA synthesis.
- VSV mutants restricted in transcription did not inhibit RNA synthesis, even at high multiplicities.
- A viral product synthesized 30-60 minutes after permissive infection was essential for sustained RNA synthesis inhibition.
Conclusions:
- VSV transcription is essential for the progressive inhibition of host cell RNA synthesis.
- A specific viral product, synthesized during permissive infection, plays a critical role in this process.
- These findings elucidate a key viral strategy for host cell manipulation.