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pH-dependent hemolysis and cell fusion of rhabdoviruses

Insights

Fungal protease or trypsin treatment makes human red blood cells susceptible to vesicular stomatitis virus (VSV) and rabies virus. These viruses cause hemolysis and fusion, particularly at acidic pH, by removing erythrocyte membrane carbohydrates.

Area of Science:

  • Virology
  • Biochemistry
  • Cell Biology

Background:

  • Vesicular stomatitis virus (VSV) and rabies virus are known to interact with host cells.
  • Erythrocyte membranes possess specific surface structures that may mediate viral interactions.

Purpose of the Study:

  • To investigate the effect of proteolytic enzymes on human erythrocyte susceptibility to VSV and rabies virus.
  • To characterize the hemolytic and fusion activities of these viruses on treated erythrocytes.
  • To elucidate the role of erythrocyte membrane carbohydrates in viral interactions.

Main Methods:

  • Human erythrocytes were pretreated with fungal semialkali protease or trypsin.
  • Treated erythrocytes were incubated with VSV and rabies virus.
  • Hemagglutination, hemolysis, and fusion assays were performed.
  • pH-dependency and virus dose-dependency were analyzed.
  • Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) was used to analyze membrane protein changes.

Main Results:

  • Protease or trypsin pretreatment rendered erythrocytes susceptible to hemagglutination by VSV and rabies virus.
  • Both viruses exhibited significant hemolytic and fusion activities on treated erythrocytes, most pronounced at pH 5.0.
  • VSV showed slight hemolytic activity at neutral pH.
  • Viral hemolysis was dose-dependent and inhibited by antiviral antibodies.
  • SDS-PAGE indicated removal of carbohydrates from erythrocyte membrane proteins post-enzyme treatment.

Conclusions:

  • Proteolytic removal of carbohydrates from erythrocyte membranes enhances susceptibility to VSV and rabies virus-induced hemolysis and fusion.
  • Viral interaction and subsequent cell damage are pH-dependent.
  • These findings highlight the role of specific erythrocyte surface carbohydrates in mediating viral entry and cytopathic effects.

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