Vaccine-induced immunopathology during bovine respiratory syncytial virus infection: exploring the parameters of pathogenesis

A.F.G. Antonis, R.S. Schrijver, F.J. Daus, M. Steverink, N. Stockhofe, J.P. Langedijk, R.G. van der Most

    Research output: Contribution to journalArticleAcademicpeer-review

    70 Citations (Scopus)

    Abstract

    The bovine and human respiratory syncytial viruses cause severe lower respiratory tract infections. Effective vaccines against the respiratory syncytial viruses have been lacking since vaccine failures in the 1960s and 1970s. In this report, we describe a bovine respiratory syncytial virus (bRSV) challenge model in which both classical bRSV respiratory infection and vaccine-enhanced immune pathology were reproduced. The classical, formalin-inactivated (FI) bRSV vaccine that has been associated with vaccine failure was efficient in inducing high antibody titers and reducing viral loads but also primed calves for a far more serious enhanced respiratory disease after a bRSV challenge, thereby mimicking the enhanced clinical situation in FI human RSV (hRSV)-immunized and hRSV-infected infants in the 1960s. We show that immunization with FI-bRSV mainly primes a Th2-like inflammatory response that is characterized by a significant eosinophilic influx in the bronchial alveolar lung fluid and lung tissues and high levels of immunoglobulin E serum antibodies. The current model may be useful in the evaluation of new bRSV candidate vaccines for potency and safety
    Original languageEnglish
    Pages (from-to)12067-12073
    JournalJournal of Virology
    Volume77
    Issue number22
    DOIs
    Publication statusPublished - 2003

    Fingerprint

    Bovine respiratory syncytial virus
    immunopathology
    Respiratory Syncytial Virus Infections
    Respiratory Syncytial Virus Vaccines
    Vaccines
    pathogenesis
    vaccines
    infection
    formalin
    Formaldehyde
    Respiratory Tract Infections
    respiratory tract diseases
    Human respiratory syncytial virus
    lungs
    Vaccine Potency
    immunoglobulin E
    Lung
    antibodies
    Antibodies
    viral load

    Keywords

    • experimental reproduction
    • inactivated vaccine
    • rsv infection
    • calves
    • disease
    • antibodies
    • pneumonia
    • children
    • infants

    Cite this

    Antonis, A.F.G. ; Schrijver, R.S. ; Daus, F.J. ; Steverink, M. ; Stockhofe, N. ; Langedijk, J.P. ; van der Most, R.G. / Vaccine-induced immunopathology during bovine respiratory syncytial virus infection: exploring the parameters of pathogenesis. In: Journal of Virology. 2003 ; Vol. 77, No. 22. pp. 12067-12073.
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    abstract = "The bovine and human respiratory syncytial viruses cause severe lower respiratory tract infections. Effective vaccines against the respiratory syncytial viruses have been lacking since vaccine failures in the 1960s and 1970s. In this report, we describe a bovine respiratory syncytial virus (bRSV) challenge model in which both classical bRSV respiratory infection and vaccine-enhanced immune pathology were reproduced. The classical, formalin-inactivated (FI) bRSV vaccine that has been associated with vaccine failure was efficient in inducing high antibody titers and reducing viral loads but also primed calves for a far more serious enhanced respiratory disease after a bRSV challenge, thereby mimicking the enhanced clinical situation in FI human RSV (hRSV)-immunized and hRSV-infected infants in the 1960s. We show that immunization with FI-bRSV mainly primes a Th2-like inflammatory response that is characterized by a significant eosinophilic influx in the bronchial alveolar lung fluid and lung tissues and high levels of immunoglobulin E serum antibodies. The current model may be useful in the evaluation of new bRSV candidate vaccines for potency and safety",
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    Vaccine-induced immunopathology during bovine respiratory syncytial virus infection: exploring the parameters of pathogenesis. / Antonis, A.F.G.; Schrijver, R.S.; Daus, F.J.; Steverink, M.; Stockhofe, N.; Langedijk, J.P.; van der Most, R.G.

    In: Journal of Virology, Vol. 77, No. 22, 2003, p. 12067-12073.

    Research output: Contribution to journalArticleAcademicpeer-review

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