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Inhibition of protein synthesis in L cells infected with vesicular stomatitis virus

Journal of Virology
|January 1, 1972
PubMed

Insights

Vesicular stomatitis virus (VSV) inhibits protein synthesis in L cells through a two-step process. This involves an early, UV-insensitive phase and a later, UV-sensitive phase, both requiring new protein synthesis post-infection.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Vesicular stomatitis virus (VSV) is known to disrupt host cell functions.
  • Protein synthesis is a critical cellular process often targeted by viral infections.
  • Understanding viral mechanisms of host protein synthesis inhibition is key to antiviral research.

Purpose of the Study:

  • To elucidate the mechanisms by which VSV inhibits protein synthesis in L cells.
  • To differentiate between distinct phases and dependencies of VSV-induced protein synthesis inhibition.

Main Methods:

  • Infection of L cells with VSV under varying conditions.
  • Assessment of protein synthesis inhibition.
  • Use of ultraviolet (UV) irradiation to probe mechanisms.
  • Multiplicity of infection (MOI) studies.

Main Results:

  • VSV-mediated inhibition of protein synthesis in L cells necessitates new protein synthesis after infection.
  • Two distinct inhibitory mechanisms were identified: an early, multiplicity-dependent, UV-insensitive inhibition, and a progressive, UV-sensitive inhibition.

Conclusions:

  • VSV employs a biphasic strategy to inhibit host cell protein synthesis.
  • Both phases of inhibition are dependent on the synthesis of new viral or cellular proteins.
  • The differential sensitivity to UV light suggests distinct molecular players in each phase.

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