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Interference with viral infection by defective RNA replicase

Y Inokuchi1, A Hirashima

  • 1Department of Molecular Biology, School of Medicine, Keio University, Tokyo, Japan.

Journal of Virology
|December 1, 1987
PubMed

Insights

Altering a key Glycine residue in the Q beta phage replicase conserved segment significantly inhibits phage proliferation by suppressing RNA synthesis. This suggests specific interference with wild-type and related phage infections.

Area of Science:

  • Molecular Biology
  • Virology
  • Enzymology

Background:

  • RNA-dependent RNA and DNA polymerases share a conserved Tyr-X-Asp-Asp motif.
  • This motif is crucial for polymerase function.

Purpose of the Study:

  • To investigate the function of the conserved Tyr-Gly-Asp-Asp segment in Q beta phage replicase.
  • To determine the in vivo effects of altering the Glycine residue at position 357.

Main Methods:

  • Site-directed mutagenesis was used to substitute Glycine-357 with Alanine, Serine, Proline, Methionine, or Valine in the Q beta replicase.
  • Replicase activity and phage proliferation were examined in vivo.

Main Results:

  • Mutations at Glycine-357 abolished replicase activity and severely inhibited Q beta and SP phage proliferation.
  • These altered replicases suppressed phage RNA synthesis.
  • Substitution at Glycine-390 had a minor inhibitory effect despite loss of replicase activity.

Conclusions:

  • The conserved Tyr-Gly-Asp-Asp segment is critical for Q beta phage replicase function.
  • Altered replicases at this conserved segment specifically interfere with wild-type and related phage infections.
  • This provides insights into phage-host interactions and potential antiviral strategies.

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