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Gene Review

PRV  -  Pseudorabies susceptibility

Sus scrofa

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Disease relevance of PRV

  • Pseudorabies virus (PRV) is a herpesvirus of swine, a member of the Alphaherpesvirinae subfamily, and the etiological agent of Aujeszky's disease [1].
  • Uptake and transneuronal passage of wild-type and attenuated strains of a swine alpha-herpesvirus (pseudorabies [PRV]) were examined in rat visual projections [2].
  • Alpha-herpesviruses constitute closely related neurotropic viruses, including herpes simplex virus in man and pseudorabies virus (PRV) in pigs [3].
  • One attenuated vaccine strain, Bartha PRV, has preferential affinity for sites of afferent synaptic contact on the cell body and dendrites and a reactive gliosis that effectively isolates the infected neurons and provides a barrier to the nonspecific spread to adjacent neurons [4].
  • Virus particles lacking gIII were indistinguishable from parental PRV virus particles by analysis of infected-cell thin sections in the electron microscope [5].

Psychiatry related information on PRV

  • In studies of transmission of PRV by cannibalism, either latently infected or acutely infected tissue was fed to both domestic and feral-derived pigs [6].
  • Once formulated, a decision-tree analysis can be adapted to the prevailing economic or epidemiologic conditions; hence, it is a useful tool in the PRV decision-making process [7].
  • The isolation of virus from alveolar macrophages provides support to the hypothesis that replication of PRV during the course of infection produces an impairment of the defense mechanisms in the respiratory tract [8].

High impact information on PRV

  • PRV infection progresses from acute infection of the respiratory epithelium to latent infection in the peripheral nervous system [1].
  • By contrast, the attenuated strain of PRV selectively infected a functionally distinct subset of retinal ganglion cells with restricted central projections [2].
  • We report that in vitro infection of swine TG neurons with the homologous swine alpha-herpesvirus PRV results in the appearance of numerous synaptophysin-positive synaptic boutons (varicosities) along the axons [3].
  • Both PRV strains infected DMV and motor neurons and then passed transneuronally to infect brainstem neurons that innervate the DMV [9].
  • After PRV inoculation of the rat stomach or pancreas, the temporal course of viral replication and induced pathology of infected neurons were assessed in the dorsal motor nucleus of the vagus (DMV) and amygdala using an antiserum generated against PRV [9].

Chemical compound and disease context of PRV

  • We have established that in the Becker strain of pseudorabies virus (PRV), the glycoprotein gIII gene is not essential for growth in cell culture [5].
  • To enhance the efficacy of a DNA vaccine against pseudorabies virus (PRV), we evaluated the adjuvant properties of plasmids coding for gamma interferon or interleukin-12, of CpG immunostimulatory motifs, and of the conventional adjuvants dimethyldioctadecylammonium bromide in water (DDA) and sulfolipo-cyclodextrin in squalene in water [10].
  • Contrary to human and swine thymidine kinases and like herpes simplex virus-1 and -2 thymidine kinases, PRV thymidine kinase phosphorylates both the natural (D-) and the unnatural (L-) thymidine enantiomers to their corresponding monophosphates with comparable efficiency [11].
  • Here, we demonstrate that US3 of the swine alphaherpesvirus pseudorabies virus (PRV) suppresses PRV-induced apoptosis in swine-testicle (ST) cells at late stages in infection, and that it protects ST cells from apoptosis induced by either sorbitol or staurosporine [12].
  • Furthermore, prior dietary CLA supplementation interacted with viral immunization (i.e. modified-live pseudorabies virus (PRV) vaccine) by enhancing both pseudorabies-specific proliferative responses of CD8alphabeta(+) PBMC and granzyme activities of PBMC [13].

Biological context of PRV

  • We used Ba-DupLac, a recombinant PRV strain, for the tracing experiments since this virus was demonstrated to exhibit much more restricted transportation kinetics than that of PRV Bartha, and is therefore more suitable for studies of neuronal plasticity [14].
  • These findings and the literature data suggest that this phenomenon may be related to the changes in the expression or to the redistribution of cell-adhesion molecules, which are known to facilitate the entrance and/or transmission of PRV into neurons [14].
  • We have shown previously that the BHV-1.1 gE and gI proteins are capable of complementing the virulence functions of PRV gE and gI in a rodent model (A. C. Knapp and L. W. Enquist, J. Virol. 71:2731-2739, 1997) [15].
  • It is among a linked group of three envelope protein genes in the unique short region of the PRV genome which are absent from the attenuated Bartha strain [16].
  • Each mutation was then crossed onto PRV by cotransfection of plasmid DNA and parental viral DNA by using gIII-specific monoclonal antibodies as selective and screening reagents [5].

Anatomical context of PRV

  • Neuronal infection with both PRV strains produced consistent alterations in astrocytes, ramified microglia, and brain macrophages that correlated spatially and temporally with progressive stages of viral replication and neuronal pathology [9].
  • Injection of PRV into the esophagus and subsequent detection using immunofluorescence found a subpopulation of neurons in the intermediate and interstitial subnuclei of the NTS [17].
  • Use of PRV as a neural tracer shows that during the buccopharyngeal phase of swallowing, vagal afferents from the pharynx and larynx and from the superior laryngeal nerve terminate in the intermediate and interstitial subnuclei of the NTS [17].
  • There were several similarities between these RNAs and the latency-associated transcripts detected in the trigeminal ganglia of swine latently infected with PRV (A. K. Cheung, J. Virol. 63: 2908-2913, 1989) [18].
  • Here we show that at least four major PRV glycoproteins (gB, gC, gD, and gE) in the plasma membrane of infected swine kidney cells and monocytes seem to be linked, since monospecific antibody-induced patching of any one of these proteins results in copatching of the others [19].

Associations of PRV with chemical compounds

  • A known function of the glycoprotein gC is to mediate attachment of PRV to target cells through distinct viral heparin-binding domains (HBDs) [20].
  • In the present study, using several PRV deletion mutants, we found that the US3 serine/threonine (S/T) protein kinase is involved in breakdown of actin stress fibers in different PRV-infected cell lines [21].
  • Expression of these RNAs was sensitive to phosphonoacetic acid, indicating that they are transcripts of PRV late genes [18].
  • We identified three isoforms of VP22 present in PRV-infected cells that can be resolved by polyacrylamide gel electrophoresis [22].
  • Previously, we demonstrated that the tyrosine-based YQRL motif at positions 902 to 905, but not the YMSI motif at positions 864 to 867 or the LL doublet at positions 887 and 888, is required for correct functioning of gB during antibody-mediated internalization of PRV cell surface-bound glycoproteins [23].

Other interactions of PRV


Analytical, diagnostic and therapeutic context of PRV


  1. Molecular biology of pseudorabies virus: impact on neurovirology and veterinary medicine. Pomeranz, L.E., Reynolds, A.E., Hengartner, C.J. Microbiol. Mol. Biol. Rev. (2005) [Pubmed]
  2. Two alpha-herpesvirus strains are transported differentially in the rodent visual system. Card, J.P., Whealy, M.E., Robbins, A.K., Moore, R.Y., Enquist, L.W. Neuron (1991) [Pubmed]
  3. Alpha-herpesvirus glycoprotein D interaction with sensory neurons triggers formation of varicosities that serve as virus exit sites. De Regge, N., Nauwynck, H.J., Geenen, K., Krummenacher, C., Cohen, G.H., Eisenberg, R.J., Mettenleiter, T.C., Favoreel, H.W. J. Cell Biol. (2006) [Pubmed]
  4. Laryngeal and respiratory protective reflexes. Altschuler, S.M. Am. J. Med. (2001) [Pubmed]
  5. Pseudorabies virus gene encoding glycoprotein gIII is not essential for growth in tissue culture. Robbins, A.K., Whealy, M.E., Watson, R.J., Enquist, L.W. J. Virol. (1986) [Pubmed]
  6. Mechanisms of transmission of Aujeszky's disease virus originating from feral swine in the USA. Hahn, E.C., Page, G.R., Hahn, P.S., Gillis, K.D., Romero, C., Annelli, J.A., Gibbs, E.P. Vet. Microbiol. (1997) [Pubmed]
  7. Financial analysis of pseudorabies control and eradication in swine. Rodrigues, C.A., Gardner, I.A., Carpenter, T.E. J. Am. Vet. Med. Assoc. (1990) [Pubmed]
  8. Study of the potential involvement of pseudorabies virus in swine respiratory disease. Iglesias, G.J., Trujano, M., Lokensgard, J., Molitor, T. Can. J. Vet. Res. (1992) [Pubmed]
  9. Spatiotemporal responses of astrocytes, ramified microglia, and brain macrophages to central neuronal infection with pseudorabies virus. Rinaman, L., Card, J.P., Enquist, L.W. J. Neurosci. (1993) [Pubmed]
  10. Protective antiviral immune responses to pseudorabies virus induced by DNA vaccination using dimethyldioctadecylammonium bromide as an adjuvant. van Rooij, E.M., Glansbeek, H.L., Hilgers, L.A., te Lintelo, E.G., de Visser, Y.E., Boersma, W.J., Haagmans, B.L., Bianchi, A.T. J. Virol. (2002) [Pubmed]
  11. Lack of stereospecificity of suid pseudorabies virus thymidine kinase. Maga, G., Verri, A., Bonizzi, L., Ponti, W., Poli, G., Garbesi, A., Niccolai, D., Spadari, S., Focher, F. Biochem. J. (1993) [Pubmed]
  12. The pseudorabies virus US3 protein kinase possesses anti-apoptotic activity that protects cells from apoptosis during infection and after treatment with sorbitol or staurosporine. Geenen, K., Favoreel, H.W., Olsen, L., Enquist, L.W., Nauwynck, H.J. Virology (2005) [Pubmed]
  13. Long-term influence of lipid nutrition on the induction of CD8(+) responses to viral or bacterial antigens. Bassaganya-Riera, J., Hontecillas, R., Zimmerman, D.R., Wannemuehler, M.J. Vaccine (2002) [Pubmed]
  14. Use of a recombinant pseudorabies virus to analyze motor cortical reorganization after unilateral facial denervation. Horváth, S., Prandovszky, E., Pankotai, E., Kis, Z., Farkas, T., Boldogköi, Z., Boda, K., Janka, Z., Toldi, J. Cereb. Cortex (2005) [Pubmed]
  15. The gE and gI homologs from two alphaherpesviruses have conserved and divergent neuroinvasive properties. Knapp, A.C., Husak, P.J., Enquist, L.W. J. Virol. (1997) [Pubmed]
  16. Role of pseudorabies virus Us9, a type II membrane protein, in infection of tissue culture cells and the rat nervous system. Brideau, A.D., Card, J.P., Enquist, L.W. J. Virol. (2000) [Pubmed]
  17. Central integration of swallow and airway-protective reflexes. Broussard, D.L., Altschuler, S.M. Am. J. Med. (2000) [Pubmed]
  18. The BamHI J fragment (0.706 to 0.737 map units) of pseudorabies virus is transcriptionally active during viral replication. Cheung, A.K. J. Virol. (1990) [Pubmed]
  19. Copatching and lipid raft association of different viral glycoproteins expressed on the surfaces of pseudorabies virus-infected cells. Favoreel, H.W., Mettenleiter, T.C., Nauwynck, H.J. J. Virol. (2004) [Pubmed]
  20. The porcine humoral immune response against pseudorabies virus specifically targets attachment sites on glycoprotein gC. Ober, B.T., Teufel, B., Wiesmüller, K.H., Jung, G., Pfaff, E., Saalmüller, A., Rziha, H.J. J. Virol. (2000) [Pubmed]
  21. Pseudorabies virus US3 protein kinase mediates actin stress fiber breakdown. Van Minnebruggen, G., Favoreel, H.W., Jacobs, L., Nauwynck, H.J. J. Virol. (2003) [Pubmed]
  22. The pseudorabies virus VP22 homologue (UL49) is dispensable for virus growth in vitro and has no effect on virulence and neuronal spread in rodents. del Rio, T., Werner, H.C., Enquist, L.W. J. Virol. (2002) [Pubmed]
  23. Internalization of pseudorabies virus glycoprotein B is mediated by an interaction between the YQRL motif in its cytoplasmic domain and the clathrin-associated AP-2 adaptor complex. Van Minnebruggen, G., Favoreel, H.W., Nauwynck, H.J. J. Virol. (2004) [Pubmed]
  24. The influence of porcine recombinant interferon-alpha 1 on pseudorabies virus infection of porcine nasal mucosa in vitro. Pol, J.M., Broekhuysen-Davies, J.M., Wagenaar, F., La Bonnardière, C. J. Gen. Virol. (1991) [Pubmed]
  25. Pseudorabies virus glycoprotein III derived from virions and infected cells binds to the third component of complement. Huemer, H.P., Larcher, C., Coe, N.E. Virus Res. (1992) [Pubmed]
  26. Interferon-gamma response of PBMC indicates productive pseudorabies virus (PRV) infection in swine. Hoegen, B., Saalmüller, A., Röttgen, M., Rziha, H.J., Geldermann, H., Reiner, G., Pfaff, E., Büttner, M. Vet. Immunol. Immunopathol. (2004) [Pubmed]
  27. Pneumonia in pigs induced by intranasal challenge exposure with pseudorabies virus and Pasteurella multocida. Fuentes, M.C., Pijoan, C. Am. J. Vet. Res. (1987) [Pubmed]
  28. Immunohistological characterization of the local cellular response directed against pseudorabies virus in pigs. Bouma, A., Zwart, R.J., De Bruin, M.G., De Jong, M.C., Kimman, T.G., Bianchi, A.T. Vet. Microbiol. (1997) [Pubmed]
  29. Correlation between precolonization of trigeminal ganglia by attenuated strains of pseudorabies virus and resistance to wild-type virus latency. Schang, L.M., Kutish, G.F., Osorio, F.A. J. Virol. (1994) [Pubmed]
  30. Induction and inhibition of apoptosis by pseudorabies virus in the trigeminal ganglion during acute infection of swine. Alemañ, N., Quiroga, M.I., López-Peña, M., Vázquez, S., Guerrero, F.H., Nieto, J.M. J. Virol. (2001) [Pubmed]
  31. L-particle production during primary replication of pseudorabies virus in the nasal mucosa of swine. Alemañ, N., Quiroga, M.I., López-Peña, M., Vázquez, S., Guerrero, F.H., Nieto, J.M. J. Virol. (2003) [Pubmed]
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