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Transcription of vesicular stomatitis virus is required to shut off cellular RNA synthesis

Journal of Virology
|April 1, 1979
PubMed

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.

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