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Updated: Jun 16, 2026

A High-throughput Cre-Lox Activated Viral Membrane Fusion Assay to Identify Inhibitors of HIV-1 Viral Membrane Fusion
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Published on: August 14, 2018

Reciprocal regulation of AKT and MAP kinase dictates virus-host cell fusion

Nishi R Sharma1, Prashant Mani, Neha Nandwani

  • 1Department of Biochemistry, University of Delhi South Campus, Benito Juarez Road, New Delhi 110021, India.

Journal of Virology
|February 19, 2010
PubMed

Insights

This study reveals how AKT1 and extracellular signal-regulated kinase (ERK) pathways counteract each other to control paramyxovirus fusion. Understanding these viral fusion signals offers a new therapeutic strategy.

Area of Science:

  • Virology
  • Cell Biology
  • Biochemistry

Background:

  • Paramyxoviridae family viruses use hemagglutinin-neuraminidase (HN) and fusion (F) proteins for host cell binding and membrane fusion.
  • Intracellular signaling pathways triggered by paramyxoviruses during infection remain largely uncharacterized.

Purpose of the Study:

  • To elucidate the roles of AKT1 and Raf/MEK/ERK signaling cascades in virus-cell fusion mediated by paramyxoviruses.
  • To investigate the regulation of these signaling pathways during viral fusion with liver cells.

Main Methods:

  • Utilized reconstituted envelopes containing Sendai virus fusion (F) or hemagglutinin-neuraminidase-fusion (HN-F) proteins.
  • Analyzed the activation of AKT1 and mitogen-activated protein kinase (MAPK) cascades, including ERK, during viral fusion.

Main Results:

  • Extracellular signal-regulated kinase (ERK) activation promotes viral fusion through ezrin-mediated cytoskeletal rearrangements.
  • AKT1 activation attenuates viral fusion by phosphorylating the F protein.
  • Demonstrated reciprocal activation of AKT1 and MAPK cascades, indicating counteractive regulation of viral fusion.

Conclusions:

  • Established a novel conceptual framework for understanding virus-cell fusion regulation by intracellular signaling pathways.
  • Identified AKT1 and ERK signaling as key regulators of paramyxovirus fusion, suggesting potential therapeutic targets.

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