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Journal of Virology, May 2004, p. 4806-4816, Vol. 78, No. 9
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.9.4806-4816.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

A Glycine-Rich Bovine Herpesvirus 5 (BHV-5) gE-Specific Epitope within the Ectodomain Is Important for BHV-5 Neurovirulence{dagger}

A. Al-Mubarak,1 Y. Zhou,2 and S. I. Chowdhury1*

Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas 66506,1 Center for Biotechnology, University of Nebraska-Lincoln, Lincoln, Nebraska 685882

Received 20 November 2003/ Accepted 9 January 2004

The bovine herpesvirus 5 (BHV-5) gE ectodomain contains a glycine-rich epitope coding region (gE5 epitope), residues 204 to 218, that is significantly different from the corresponding gE region of BHV-1. Deletion of the gE epitope significantly reduced the neurovirulence of BHV-5 in rabbits. Pulse-chase analyses revealed that the epitope-deleted and wild-type gE were synthesized as N-glycosylated endoglycosidase H-sensitive precursors with approximate molecular masses of 85 kDa and 86 kDa, respectively. Like the wild-type gE, epitope-deleted gE complexed with gI and was readily transported from the endoplasmic reticulum. Concomitantly, the epitope-deleted and wild-type gE acquired posttranslational modifications in the Golgi leading to an increased apparent molecular mass of 93-kDa (epitope-deleted gE) and 94-kDa (wild-type gE). The kinetics of mutant and wild-type gE processing were similar, and both mature proteins were resistant to endoglycosidase H but sensitive to glycopeptidase F. The gE epitope-deleted BHV-5 formed wild-type-sized plaques in MDBK cells, and the epitope-deleted gE was expressed on the cell surface. However, rabbits infected intranasally with gE epitope-deleted BHV-5 did not develop seizures, and only 20% of the infected rabbits showed mild neurological signs. The epitope-deleted virus replicated efficiently in the olfactory epithelium. However, within the brains of these rabbits there was a 10- to 20-fold reduction in infected neurons compared with the number of infected neurons within the brains of rabbits infected with the gE5 epitope-reverted and wild-type BHV-5. In comparison, 70 to 80% of the rabbits exhibited severe neurological signs when infected with the gE5 epitope-reverted and wild-type BHV-5. These results indicated that anterograde transport of the gE epitope-deleted virus from the olfactory receptor neurons to the olfactory bulb is defective and that, within the central nervous system, the gE5 epitope-coding region was required for expression of the full virulence potential of BHV-5.

* Corresponding author. Mailing address: Department of Diagnostic Medicine/Pathobiology, College of Veterinary Medicine, Kansas State University, Manhattan, KS 66506. Phone: (785) 532-4616. Fax: (785) 532-4851. E-mail: Chowdh{at}vet.k-state.edu.

{dagger} Contribution 03-236-J, Kansas Agricultural Experiment Station.

Journal of Virology, May 2004, p. 4806-4816, Vol. 78, No. 9
0022-538X/04/$08.00+0     DOI: 10.1128/JVI.78.9.4806-4816.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Liu, Z. F., Brum, M. C. S., Doster, A., Jones, C., Chowdhury, S. I. (2008). A Bovine Herpesvirus Type 1 Mutant Virus Specifying a Carboxyl-Terminal Truncation of Glycoprotein E Is Defective in Anterograde Neuronal Transport in Rabbits and Calves. J. Virol. 82: 7432-7442 [Abstract] [Full Text]  
  • Brower, A., Homb, K. M., Bochsler, P., Porter, R., Woods, K., Ubl, S., Krueger, D., Cigel, F., Toohey-Kurth, K. (2008). Encephalitis in aborted bovine fetuses associated with Bovine herpesvirus 1 infection. jvdi 20: 297-303 [Abstract] [Full Text]  
  • Chowdhury, S. I., Mahmood, S., Simon, J., Al-Mubarak, A., Zhou, Y. (2006). The Us9 Gene of Bovine Herpesvirus 1 (BHV-1) Effectively Complements a Us9-Null Strain of BHV-5 for Anterograde Transport, Neurovirulence, and Neuroinvasiveness in a Rabbit Model. J. Virol. 80: 4396-4405 [Abstract] [Full Text]  


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