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Inhibition of late influenza virus genome expression by diamidinophenylindole

G Conti1, P Portincasa, C Chezzi

  • 1Instituto di Microbiologia, Facoltà di Medicina e Chirurgia, Università delgi Studi, Parma, Italy.

Annales De L'Institut Pasteur. Virology
|January 1, 1988
PubMed

Insights

Diamidinophenylindole (DAPI) treatment alters influenza virus replication in LLC-MK2 cells, restricting viral protein synthesis and blocking replication. DAPI likely targets late viral genome transcription, offering a model for studying cellular intervention in virus growth.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Influenza virus replication is a complex process involving intricate interactions between viral and cellular machinery.
  • Understanding the molecular mechanisms that regulate viral gene expression is crucial for developing antiviral strategies.

Purpose of the Study:

  • To investigate the effects of diamidinophenylindole (DAPI) on the replication cycle of influenza virus strain FPV, Ulster 73.
  • To elucidate the specific stage of viral replication targeted by DAPI and its impact on viral gene expression.

Main Methods:

  • Treatment of LLC-MK2 cells with DAPI during influenza virus infection.
  • Analysis of viral protein synthesis patterns.
  • Kinetic studies on viral RNA production.
  • Assessment of viral replication progression post-treatment.

Main Results:

  • DAPI treatment restricted viral protein synthesis to an early pattern.
  • The drug blocked virus replication until 4 hours post-infection.
  • Inhibition of late viral product synthesis, particularly membrane proteins, was observed.
  • DAPI reduced the synthesis of late virus-induced RNA species, suggesting a target in late transcription.

Conclusions:

  • Diamidinophenylindole (DAPI) interferes with late-stage influenza virus transcription and replication.
  • The nonpermissive state induced by DAPI provides a model for studying cellular involvement in viral growth.

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