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Failure to activate the IFN-β promoter by a paramyxovirus lacking an interferon antagonist

M J Killip1, D F Young, C S Ross

  • 1School of Biology, Centre for Biomolecular Sciences, North Haugh, University of St. Andrews, St. Andrews, Fife, UK.

Virology
|April 23, 2011
PubMed

Insights

Parainfluenza virus type 5 (PIV5) infection does not typically produce pathogen-associated molecular patterns (PAMPs) that trigger interferon (IFN) induction. Instead, defective viruses appear to be the main cause of IFN activation during PIV5 infection.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Pathogen-associated molecular patterns (PAMPs) are thought to be produced during viral replication and trigger interferon (IFN) induction.
  • Viruses often encode antagonists to limit the activation of the IFN response by PAMPs.

Purpose of the Study:

  • To investigate the induction of IFN by parainfluenza virus type 5 (PIV5) at the single-cell level.
  • To determine the role of the PIV5 V protein in IFN induction.

Main Methods:

  • Utilized a cell line engineered to express GFP under the control of the IFN-β promoter.
  • Infected cells with a recombinant PIV5 lacking a functional V protein (PIV5-VΔC).
  • Monitored GFP expression as a readout for IFN-β promoter activation.

Main Results:

  • PIV5-VΔC, lacking the viral IFN antagonist V protein, failed to activate the IFN-β promoter in most infected cells.
  • This suggests that PAMPs capable of activating IFN induction are not produced or exposed during normal PIV5 replication.
  • Interferon induction during PIV5 infection is likely triggered by defective viral particles.

Conclusions:

  • Viral PAMPs are not the primary inducers of IFN during standard PIV5 replication.
  • Defective PIV5 particles are implicated as the main drivers of IFN induction in this model system.
  • The PIV5 V protein plays a crucial role in antagonizing IFN induction.

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