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Low-pH-induced fusion of Vero cells infected with Junin virus

V Castilla1, S E Mersich

  • 1Laboratorio de Virologia, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.

Archives of Virology
|January 1, 1996
PubMed

Insights

Junin virus (JV) causes cell fusion in a pH and temperature-dependent manner. Neutralizing antibodies targeting the viral glycoprotein (GP38) block this fusion process, indicating GP38

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Junin virus (JV) is an arenavirus responsible for Argentinian hemorrhagic fever.
  • Understanding JV's cell-to-cell fusion mechanism is crucial for developing antiviral strategies.
  • Viral glycoproteins often mediate cell fusion, a key step in viral entry and spread.

Purpose of the Study:

  • To investigate the capacity of Junin virus to induce cell-cell fusion.
  • To determine the factors influencing JV-mediated syncytia formation.
  • To elucidate the role of the viral glycoprotein (GP38) in the fusion process.

Main Methods:

  • Infection of Vero and BHK-21 cells with Junin virus.
  • Assessment of polykaryocyte (syncytia) formation under varying pH and temperature conditions.
  • Immunoprecipitation assays to detect conformational changes in GP38 upon acid treatment.
  • Inhibition assays using neutralizing antibodies against GP38.

Main Results:

  • Junin virus infection induced significant cell-cell fusion (polykaryocyte formation) in Vero cells.
  • Fusion activity was dependent on both pH and temperature.
  • BHK-21 cells showed reduced susceptibility to JV-induced fusion.
  • Different JV strains displayed similar fusion extent and pH dependence.
  • Neutralizing antibodies against GP38 effectively inhibited syncytium production.
  • GP38 exhibited conformational changes when exposed to acidic conditions.

Conclusions:

  • Junin virus possesses a potent cell-cell fusion capacity mediated by its glycoprotein, GP38.
  • The fusion process is regulated by environmental factors like pH and temperature.
  • GP38 undergoes acid-induced conformational changes, suggesting a role in membrane fusion.
  • Targeting GP38 with neutralizing antibodies is a viable strategy to inhibit JV spread.

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