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Hijacking components of the cellular secretory pathway for replication of poliovirus RNA

George A Belov1, Nihal Altan-Bonnet, Gennadiy Kovtunovych

  • 1National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8011, USA.

Journal of Virology
|November 3, 2006
PubMed

Insights

Poliovirus infection hijacks cellular Arf GTPase pathways. Viral proteins recruit specific Arf GEFs, essential for forming replication complexes and enabling virus propagation.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Poliovirus infection causes significant cellular membrane reorganization, forming replication sites.
  • The precise mechanisms of this membrane remodeling and the involved cellular pathways are not fully understood.
  • Small GTPases of the Arf family regulate cellular trafficking and have been observed to associate with poliovirus replication complexes.

Purpose of the Study:

  • To elucidate the role of Arf GTPases and their regulators in poliovirus-induced membrane reorganization.
  • To identify the specific viral components responsible for recruiting Arf pathway members.
  • To understand the contribution of Arf pathway activation to viral RNA replication.

Main Methods:

  • Investigated the association of Arf GTPases with viral RNA replication complexes in infected cells.
  • Utilized in vitro assays to study the binding of Arf proteins after poliovirus protein synthesis.
  • Examined the recruitment of Arf guanine nucleotide exchange factors (GEFs) by specific viral proteins.
  • Assessed the impact of brefeldin A on poliovirus growth and the effect of GBF1 overexpression.

Main Results:

  • Two distinct poliovirus proteins were found to independently recruit different Arf GEFs (GBF1 and BIG1/2) to replication structures.
  • Intracellular levels of active Arf-GTP increased approximately fourfold during poliovirus infection.
  • Virus growth sensitivity to brefeldin A was linked to the requirement for specific GEFs and could be rescued by GBF1 overexpression.

Conclusions:

  • Poliovirus proteins actively recruit specific Arf GEFs, GBF1 and BIG1/2, to orchestrate membrane remodeling for viral RNA replication.
  • The observed increase in Arf-GTP levels highlights the critical role of Arf pathway activation in the viral life cycle.
  • Understanding this recruitment mechanism provides key insights into the cellular pathways exploited by poliovirus to establish its replication factories.

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