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Gene Review

UL23  -  thymidine kinase

Suid herpesvirus 1

 
 
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Disease relevance of UL23

  • An analysis of recombinants between the Bartha vaccine strain and a virulent pseudorabies virus strain (having or lacking a thymidine kinase gene [TK+ or TK-]) revealed the following [1].
  • One virus, PRV delta GX1, was derived by insertion of the herpes simplex virus thymidine kinase gene into the gX-coding region [2].
  • In order to prevent reversion and also to enable identification of the modified virus, a "marker" transcriptional unit (Escherichia coli lacZ gene fused to a SV-40 3'-polyadenylation signal sequence and regulated by the pseudorabies virus gX gene promoter) was inserted via homologous recombination at one of two loci within the ILTV TK gene [3].
  • Since the thymidine kinase (TK) activity of herpesviruses has been associated with virulence, inactivation of the encoding gene in the ILTV genome should attenuate the virus [3].
  • During a study designed to identify changes in the genomes that are observed in mutant populations of pseudorabies virions, a thymidine kinase-defective population of virions which contains genomes that possess inverted repeated sequences of unequal sizes has been identified [4].
 

High impact information on UL23

  • To further our knowledge, pseudorabies virus, attenuated by deletion of the glycoprotein E gene to impair its neurovirulence and by deletion of the thymidine kinase gene (gE-TK-PRV), was used to infect wild-type 129Sv/Ev and congenic mice with immune system-associated genetic deficiencies [5].
  • The in vitro secondary CTL response of lymphocytes obtained from either mice or pigs 6 or more weeks after immunization with a TK- mutant of PrV was also tested [6].
  • These results indicate that both thymidine kinase activity and an intact US were necessary but not sufficient for the expression of virulence [1].
  • Inactivation of TK and RR, but not inactivation of gE, gG or PK, severely affected the replication in both monocytes and lymphocytes [7].
  • PK and TK have thus far not been reported to induce B or T cell responses [8].
 

Biological context of UL23

 

Anatomical context of UL23

  • This study indicated the probable importance of PRV TK expression in acute trigeminal ganglion infection [9].
  • Histologic lesions were found in the respiratory and the central nervous systems, however, the lesions in the TK- mutant-inoculated pigs were much milder compared to those registered for the control pigs [12].
 

Associations of UL23 with chemical compounds

 

Analytical, diagnostic and therapeutic context of UL23

References

  1. Genetic basis of the neurovirulence of pseudorabies virus. Lomniczi, B., Watanabe, S., Ben-Porat, T., Kaplan, A.S. J. Virol. (1984) [Pubmed]
  2. Replication and virulence of pseudorabies virus mutants lacking glycoprotein gX. Thomsen, D.R., Marchioli, C.C., Yancey, R.J., Post, L.E. J. Virol. (1987) [Pubmed]
  3. Generation of thymidine kinase-deficient mutants of infectious laryngotracheitis virus. Schnitzlein, W.M., Winans, R., Ellsworth, S., Tripathy, D.N. Virology (1995) [Pubmed]
  4. Equalization of the inverted repeat sequences of the pseudorabies virus genome by intermolecular recombination. Ben-Porat, T., Deatly, A., Veach, R.A., Blankenship, M.L. Virology (1984) [Pubmed]
  5. Role of the individual interferon systems and specific immunity in mice in controlling systemic dissemination of attenuated pseudorabies virus infection. Grob, P., Schijns, V.E., van den Broek, M.F., Cox, S.P., Ackermann, M., Suter, M. J. Virol. (1999) [Pubmed]
  6. Pseudorabies virus glycoprotein gIII is a major target antigen for murine and swine virus-specific cytotoxic T lymphocytes. Zuckermann, F.A., Zsak, L., Mettenleiter, T.C., Ben-Porat, T. J. Virol. (1990) [Pubmed]
  7. Role of viral proteins and concanavalin A in in vitro replication of pseudorabies virus in porcine peripheral blood mononuclear cells. Mulder, W.A., Priem, J., Pol, J.M., Kimman, T.G. J. Gen. Virol. (1995) [Pubmed]
  8. Inactivation of glycoprotein gE and thymidine kinase or the US3-encoded protein kinase synergistically decreases in vivo replication of pseudorabies virus and the induction of protective immunity. Kimman, T.G., De Wind, N., De Bruin, T., de Visser, Y., Voermans, J. Virology (1994) [Pubmed]
  9. The role of pseudorabies virus thymidine kinase expression in trigeminal ganglion infection. Tenser, R.B., Ressel, S.J., Fralish, F.A., Jones, J.C. J. Gen. Virol. (1983) [Pubmed]
  10. Loss of pseudorabies virus thymidine kinase activity due to a single base mutation and amino acid substitution. Prieto, J., Martín Hernández, A.M., Tabarés, E. J. Gen. Virol. (1991) [Pubmed]
  11. Multiple sets of adjacent mu E1 and oct-1 binding sites upstream of the pseudorabies virus immediate-early gene promoter. Kozmík, Z., Arnold, L., Paces, V. Virology (1991) [Pubmed]
  12. The response of pigs inoculated with a thymidine kinase-negative (TK-) pseudorabies virus to challenge infection with virulent virus. Ferrari, M., Gualandi, G.L., Corradi, A., Monaci, C., Romanelli, M.G., Losio, M.N., Cantoni, A.M., Pratelli, A. Comp. Immunol. Microbiol. Infect. Dis. (2000) [Pubmed]
  13. Efficacy of a pseudorabies virus vaccine based on deletion mutant strain 783 that does not express thymidine kinase and glycoprotein I. van Oirschot, J.T., Moormann, R.J., Berns, A.J., Gielkens, A.L. Am. J. Vet. Res. (1991) [Pubmed]
  14. Vaccination of swine with thymidine kinase-deficient mutants of pseudorabies virus. McGregor, S., Easterday, B.C., Kaplan, A.S., Ben-Porat, T. Am. J. Vet. Res. (1985) [Pubmed]
  15. Genotypic screening of pseudorabies virus strains for thymidine kinase deletions by use of the polymerase chain reaction. Dangler, C.A., Deaver, R.E., Kolodziej, C.M., Rupprecht, J.D. Am. J. Vet. Res. (1992) [Pubmed]
  16. Construction of bovine herpesvirus-1 (BHV-1) recombinants which express pseudorabies virus (PRV) glycoproteins gB, gC, gD, and gE. Otsuka, H., Xuan, X. Arch. Virol. (1996) [Pubmed]
  17. Comparison of protection levels against pseudorabies virus infection of transgenic mice expressing a soluble form of porcine nectin-1/HveC and vaccinated mice. Ono, E., Tomioka, Y., Taharaguchi, S., Cherel, P. Vet. Microbiol. (2006) [Pubmed]
 
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