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Pseudorabies virus infections in explants of porcine nasal mucosa

J M Pol1, W G Quint, G L Kok

  • 1Central Veterinary Institute, Virology Department, Lelystad, The Netherlands.

Insights

Virulent pseudorabies virus (PRV) strains spread rapidly in porcine nasal mucosa, causing necrosis. Less virulent strains replicate slower and remain localized, indicating viral virulence correlates with replication speed.

Area of Science:

  • Veterinary Virology
  • Infectious Disease Pathogenesis
  • Porcine Health

Background:

  • Pseudorabies virus (PRV) causes significant economic losses in swine production.
  • Understanding PRV strain variation in virulence and spread is crucial for disease control.
  • Porcine nasal mucosa is a primary site for PRV entry and initial replication.

Purpose of the Study:

  • To compare the infectivity and morphogenesis of three PRV strains in porcine nasal mucosa explants.
  • To elucidate the relationship between viral replication, cell tropism, and virulence.
  • To investigate the mechanisms of PRV spread within the nasal epithelium and underlying stroma.

Main Methods:

  • Organ culture of porcine nasal mucosa explants.
  • Infection with virulent NIA-3 strain, deletion mutant 2.4N3A, and non-virulent Bartha strain of PRV.
  • Electron microscopy for observing viral morphogenesis and cell entry.
  • In situ DNA hybridization for detecting viral DNA accumulation.

Main Results:

  • All three PRV strains infected nasal epithelial cells.
  • Virulent NIA-3 enveloped at the inner nuclear membrane, rapidly invaded stroma, causing necrosis.
  • Mutant 2.4N3A and Bartha virus enveloped at the endoplasmic reticulum, with slower spread.
  • Bartha virus infection remained restricted to epithelial cells; DNA accumulated in the nucleus.
  • Viral virulence correlated directly with replication and release speed from infected cells.

Conclusions:

  • PRV strain virulence in nasal mucosa is linked to replication kinetics and cell-to-cell spread.
  • Differences in envelopment sites (nuclear membrane vs. endoplasmic reticulum) influence viral pathogenesis.
  • Understanding these mechanisms can inform strategies for PRV vaccine development and control.

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