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The PI3K/Akt pathway contributes to arenavirus budding

Shuzo Urata1, Nhi Ngo, Juan Carlos de la Torre

  • 1Department of Immunology and Microbial Science IMM-6, The Scripps Research Institute, La Jolla, California, USA.

Journal of Virology
|February 21, 2012
PubMed

Insights

Targeting the PI3K/Akt pathway inhibits lymphocytic choriomeningitis virus (LCMV) replication by affecting viral budding and RNA synthesis. This suggests a novel antiviral strategy for arenavirus infections.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Arenaviruses, including Lassa virus (LASV), cause significant human hemorrhagic fever (HF).
  • Lymphocytic choriomeningitis virus (LCMV), a globally distributed arenavirus, is a neglected human pathogen.
  • The phosphatidylinositol 3-kinase (PI3K)/Akt pathway is crucial for cellular processes and viral replication.

Purpose of the Study:

  • To investigate the role of the PI3K/Akt pathway in the life cycle of LCMV.
  • To evaluate the potential of PI3K/Akt pathway inhibition as an antiviral strategy against LCMV.

Main Methods:

  • Inhibition of the PI3K/Akt pathway in cultured cells infected with LCMV.
  • Assessment of viral RNA synthesis and budding upon pathway inhibition.
  • Treatment of LCMV-infected cells with BEZ-235, a PI3K inhibitor.

Main Results:

  • Inhibition of the PI3K/Akt pathway significantly reduced LCMV budding and, to a lesser extent, RNA synthesis.
  • Cell entry of LCMV was not affected by PI3K/Akt pathway inhibition.
  • The PI3K inhibitor BEZ-235 effectively inhibited LCMV multiplication in cell culture.

Conclusions:

  • The PI3K/Akt pathway is essential for LCMV replication, particularly for viral budding.
  • Targeting the PI3K/Akt pathway represents a promising antiviral approach for human-pathogenic arenaviruses, including LCMV and Junin virus (JUNV).

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