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Border disease. Virus-induced decrease in thyroid hormone levels with associated hypomyelination.

C A Anderson, R J Higgins, M E Smith

    Laboratory Investigation; a Journal of Technical Methods and Pathology
    |August 1, 1987
    PubMed
    Summary
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    Border disease virus (BDV) infection in pregnant sheep caused congenital hypomyelination in lambs. This spinal cord lesion may result from BDV-induced thyroid hormone deficiency due to thyroid gland infection.

    Area of Science:

    • Veterinary Virology
    • Neuroscience
    • Endocrinology

    Background:

    • Border disease (BD) is a congenital demyelinating condition in sheep.
    • Border disease virus (BDV) is the causative agent, often transmitted in utero.
    • The pathogenesis of BD-associated hypomyelination is not fully understood.

    Purpose of the Study:

    • To investigate the role of viral infection in the thyroid and pituitary glands of lambs with Border disease.
    • To determine if viral infection affects hormone levels and myelin development in the central nervous system.

    Main Methods:

    • Lambs were infected in utero with BDV isolate #31.
    • Immunocytochemistry and immunofluorescence were used to detect BDV antigen in spinal cord, thyroid, and pituitary tissues.
    • Serum hormone concentrations (thyroxine, triiodothyronine, growth hormone, thyroid-stimulating hormone) and spinal cord enzyme activity were measured.

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    Main Results:

    • Clinically affected lambs exhibited spinal cord hypomyelination.
    • BDV antigen was detected in thyroid follicular cells and pituitary cells (containing growth hormone, ACTH, prolactin, LH).
    • BD lambs showed significantly lower serum thyroxine and triiodothyronine levels and reduced spinal cord enzyme activity (2',3'-cyclic nucleotide-3'-phosphodiesterase).

    Conclusions:

    • Results suggest that BDV-induced hypomyelination may be linked to depressed thyroid hormone levels.
    • The thyroid gland is infected by BDV without apparent morphologic damage.
    • This study highlights a potential mechanism of virus-induced hormonal alteration causing congenital lesions in animals.