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Inhibition of interjacent ribonucleic acid (26S) synthesis in cells infected by Sindbis virus

Journal of Virology
|August 1, 1969
PubMed

Insights

Sindbis virus infection shows that viral RNA synthesis is linked to protein synthesis. Inhibiting protein synthesis early stops intermediate RNA production, but the resulting RNA remains biologically active.

Area of Science:

  • Virology
  • Molecular Biology
  • Biochemistry

Background:

  • Sindbis virus is an RNA virus that infects cells and hijacks their machinery for replication.
  • Understanding the interplay between viral RNA and protein synthesis is crucial for comprehending viral replication cycles.

Purpose of the Study:

  • To investigate the relationship between viral ribonucleic acid (RNA) and protein synthesis in Sindbis virus-infected cells.
  • To determine if viral RNA synthesis is dependent on concurrent protein synthesis.

Main Methods:

  • Utilizing puromycin to inhibit protein synthesis early in Sindbis virus infection.
  • Employing temperature-sensitive mutants of Sindbis virus to control RNA synthesis.
  • Analyzing the biological activity of viral RNA produced under inhibited conditions.

Main Results:

  • Early inhibition of protein synthesis with puromycin preferentially blocked the synthesis of intermediate-sized viral RNA (26S).
  • Similar inhibition of 26S RNA synthesis was observed when using a temperature-sensitive Sindbis virus mutant.
  • Viral RNA synthesized under these inhibitory conditions was found to be biologically active.
  • Established viral RNA synthesis in wild-type Sindbis infections did not necessitate ongoing protein synthesis.

Conclusions:

  • Viral RNA synthesis and protein synthesis are interdependent, particularly in the early stages of Sindbis virus infection.
  • The synthesis of intermediate viral RNA (26S) is sensitive to protein synthesis inhibition.
  • Viral RNA produced during inhibited protein synthesis remains functional, suggesting a complex regulatory mechanism.

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