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Replication and virulence of pseudorabies virus mutants lacking glycoprotein gX

Journal of Virology
|January 1, 1987
PubMed

Insights

Pseudorabies virus (PRV) glycoprotein gX was studied by creating viruses lacking functional gX. PRV delta GX1, lacking gX, demonstrated significant virulence in mice, indicating gX may play a role in modulating PRV pathogenicity.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Pseudorabies virus (PRV) is an important pathogen affecting swine and other animals.
  • PRV glycoprotein gX is known to accumulate in the medium of infected cells, suggesting a potential role in viral egress or host interaction.
  • The precise function of PRV gX in viral pathogenesis remains largely uncharacterized.

Purpose of the Study:

  • To investigate the functional role of PRV glycoprotein gX.
  • To generate and characterize PRV mutants lacking a functional gX gene.
  • To assess the virulence of gX-deficient PRV in a murine model.

Main Methods:

  • Construction of two PRV deletion mutants: PRV delta GX1 (gX-coding region insertion) and PRV delta GXTK- (subsequent deletion of inserted gene).
  • Replication assays in cell cultures to confirm viral growth and absence of gX expression.
  • Determination of the 50% lethal dose (LD50) of PRV delta GX1 in mice.

Main Results:

  • Both PRV delta GX1 and PRV delta GXTK- replicated effectively in cell culture.
  • Neither constructed virus produced detectable levels of PRV glycoprotein gX.
  • PRV delta GX1 exhibited high virulence in mice, with an LD50 of less than 100 PFU.

Conclusions:

  • The absence of functional PRV gX does not impede viral replication in cell culture.
  • PRV glycoprotein gX appears to play a role in modulating the virulence of Pseudorabies virus in vivo.
  • Further studies are warranted to elucidate the specific mechanisms by which gX influences PRV pathogenicity.

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