Poliovirus infection without accumulation of eclipse particles

O Ofori-Anyinam1, R Vrijsen, P Kronenberger

  • 1Department of Microbiology and Hygiene, Vrije Universiteit Brussel, Belgium.

Antiviral Research
|January 1, 1995
PubMed

Insights

Pyridazinamine R 78206 prevents poliovirus particle formation and delays protein synthesis. This suggests poliovirus infection doesn't require intracellular eclipse particles for replication.

Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Poliovirus replication involves complex assembly of viral particles.
  • The role of intracellular eclipse particles in poliovirus infection is not fully understood.

Purpose of the Study:

  • To investigate the effect of capsid-binding pyridazinamine R 78206 on poliovirus replication.
  • To determine if intracellular accumulation of 135 S eclipse particles is essential for poliovirus infection.

Main Methods:

  • Poliovirus type 1 (Mahoney) was treated with R 78206.
  • HeLa cells were infected with R 78206-pretreated poliovirus.
  • Viral protein synthesis and progeny virus formation were monitored.

Main Results:

  • R 78206 completely inhibited the formation of intra- and extracellular modified poliovirus particles.
  • A small amount of empty capsids was observed.
  • Viral protein synthesis and first-cycle progeny virus production were delayed by approximately 1 hour.

Conclusions:

  • The capsid-binding compound R 78206 effectively disrupts poliovirus particle assembly.
  • Poliovirus infection can proceed without the intracellular accumulation of 135 S eclipse particles, challenging previous hypotheses.

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