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Novel pneumoviruses (PnVs): Evolution and inflammatory pathology

Stephanie F Glineur1, Randall W Renshaw, Caroline M Percopo

  • 1Inflammation Immunobiology Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1883, USA.

Virology
|June 15, 2013
PubMed

Insights

This study characterizes new canine pneumovirus (PnV) isolates, revealing distinct G/glycoprotein sequences and varied immune responses in mice. Phylogenetic analysis suggests PnV groups A and B, with differing cytokine production and neutrophil recruitment.

Area of Science:

  • Veterinary Virology
  • Comparative Pathology
  • Molecular Evolution

Background:

  • A novel canine pneumovirus (PnV) shows homology to the rodent pathogen pneumonia virus of mice (PVM).
  • Previous studies indicated PnV replicates in mice but causes less mortality than PVM.

Purpose of the Study:

  • To analyze the phylogeny of 10 new PnV isolates.
  • To investigate the physiological responses of mice to these new PnV isolates.

Main Methods:

  • Phylogenetic analysis of G/glycoprotein sequences.
  • Assessment of cytokine production and neutrophil recruitment in mouse lungs.
  • Analysis of G/glycoprotein and F/fusion protein sequence pairs for positive selection.

Main Results:

  • PnV G/glycoprotein sequences exhibit elongated amino-termini compared to PVMs, suggesting division into groups A and B.
  • Significant differences in cytokine production and neutrophil recruitment were observed between group A and group B PnV isolates in BALB/c mice.
  • No evidence of positive selection (dN > dS) was found in the G/glycoprotein or F/fusion protein sequences among PnV, PVM/PnV, or PVM/PVM pairs.

Conclusions:

  • New canine pneumovirus isolates possess distinct genetic features and elicit differential host immune responses in mice.
  • The findings support the classification of PnVs into at least two groups based on G/glycoprotein characteristics.
  • Evolutionary analysis indicates a lack of positive selection in key viral proteins, suggesting conserved evolutionary pressures.
Keywords:
ChemokineInflammationNeutrophilType I interferon

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