Pseudorabies virus (PRV) is an alpha herpesvirus native to pigs that infects the peripheral nervous system and establishes a latent infection, allowing for future reactivation. Infection by PRV in non-native species such as dog and cattle leads to the rabies-like symptoms of Aujezsky’s disease including: severe phantom itch, genital infection and death. Unlike with bovine herpesvirus (BoHV-1), where the UL47 gene product has been shown to down-regulate host cells’ anti-viral defenses, the mechanism by which PRV modulates host defense is not yet fully understood. In this study, we characterize the role of the PRV UL47 gene product, VP13/14, in epithelial cell infection, and we propose VP13/14 may play a role in reducing the IFN-β response in host cells. At late time points of in vitro PRV infection, phosphorylation of STAT1 is reduced. STAT1 is a transcription factor that triggers host defenses in response to IFN-β. While UL47 plays a role in infection and appears to effect phosphorylation of STAT1, its mechanism remains to be explained. A UL47 null virus and a C-terminal UL47-GFP fusion virus were reconstituted from bacterial artificial chromosomes and characterized. While showing otherwise normal protein expression of several major viral proteins, both viruses exhibited a small plaque phenotype. Furthermore, the UL47 null virus demonstrated a log deficiency in titer at 24 hours post infection.
http://arks.princeton.edu/ark:/88435/dsp01pz50gz71q