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Mechanism of interference mediated by human parainfluenza virus type 3 infection

M A Horga1, G L Gusella, O Greengard

  • 1Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029-6574, USA.

Journal of Virology
|November 23, 2000
PubMed

Insights

Viral interference in human parainfluenza virus type 3 (HPF3) is mediated by the neuraminidase enzyme activity of the hemagglutinin-neuraminidase (HN) glycoprotein. Active HN prevents HPF3 infection by interfering with viral attachment.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Viral interference describes infected cells' resistance to subsequent viral infections.
  • Mechanisms of viral interference for human parainfluenza virus type 3 (HPF3) remain uncharacterized.
  • The role of the hemagglutinin-neuraminidase (HN) glycoprotein's neuraminidase activity in HPF3 interference is unknown.

Purpose of the Study:

  • To investigate whether continuous HN expression leads to viral receptor depletion, preventing HPF3 entry and cell fusion.
  • To determine if HPF3-infected cells expressing wild-type HN are resistant to viral infection.
  • To assess the specific contribution of neuraminidase activity to HPF3-mediated viral interference.

Main Methods:

  • Stable expression of wild-type and neuraminidase-deficient HPF3 HN-green fluorescent protein (GFP) variants on cell membranes.
  • Quantification of HN expression levels, cell surface neuraminidase activity, and resistance to HPF3 infection.
  • Comparison of infection resistance between cells expressing wild-type HN and those expressing a neuraminidase-deficient HN variant.

Main Results:

  • A correlation was established between the level of HN expression, neuraminidase activity, and protection from HPF3 infection.
  • Cells with higher HN expression and surface neuraminidase activity showed increased resistance to HPF3 infection.
  • Cells expressing a neuraminidase-deficient HN variant were not protected from infection, even with high HN surface expression.

Conclusions:

  • HPF3 HN-mediated viral interference is directly attributable to active neuraminidase enzyme activity.
  • This study provides the first definitive evidence that viral neuraminidase mediates attachment interference in paramyxoviruses.
  • The findings elucidate a key mechanism of viral resistance in HPF3 infections.

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