Experimental infection of calves with a gI, gE, US9 negative bovine herpesvirus type 5

S.O. Hubner, A.P. Oliveira, A.C. Franco, F.A.M. Rijsewijk, P.M. Roehe

    Research output: Contribution to journalArticleAcademicpeer-review

    14 Citations (Scopus)

    Abstract

    In this work, a role for the genes encoding glycoproteins I (gI) and E (gE) and the US9 protein of bovine herpesvirus type 5 (BHV-5) in neuropathogenicity and reactivation of latent infections was examined. Calves infected intranasally with a gI/gE/US9 deleted recombinant shed up to 102.85 TCID50/ml infectious virus in nasal secretions. Calves infected with the wild type BHV-5 parental virus shed up to 105 TCID50/ml virus. No signs of disease were observed in calves infected with the recombinant virus, whereas those infected with wild type virus displayed respiratory and neurological signs. The recombinant was only able to reach the basal portions of the central nervous system. In contrast, wild type virus was found widespread within the brain. Reactivation with dexamethasone 60 days post-infection resulted in reactivation of wild type virus, whereas the recombinant virus could not be reactivated. These studies demonstrate that genes gI, gE and US9 of BHV-5 are important for its neuropathogenicity and its ability to reactive from latency
    Original languageEnglish
    Pages (from-to)187-196
    JournalComparative Immunology Microbiology and Infectious Diseases
    Volume28
    Issue number3
    DOIs
    Publication statusPublished - 2005

    Keywords

    • neurological disease
    • glycoprotein-e
    • virus
    • virulence
    • bhv-5
    • immunogenicity
    • pathogenesis
    • reactivation
    • deletion
    • rabbits

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