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HAM rat, an animal model of HAM/TSP in humans Takashi YOSHIKI 1 1Department of Pathology I, Hokkaido University School of Medicine pp.946-953
Published Date 1993/12/10
DOI https://doi.org/10.11477/mf.1431900386
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Both seronegative and seropositive HTLV-I carrier rats of WKAH strain develop chronic progressive spastic paraparesis of the hind legs, after long incubation periods of 16 months. The clinical symptoms and neuropathology of seropositive adult carriers are basically identical to, but are apparently milder than those of seronegative newborn carriers. Humoral antibodies to HTLV-I in the host, therefore, do not play an active role in the pathogenesis of rat HAM. Rather, production of humoral antibodies to HTLV-I may be self-protective against disease progression. Seronegative and seropositive carriers of other strains, LEW, F344, ACI, BUF, SDJ, and LEJ do not develop rat HAM clinically and pathologically at comparable ages. It is concluded that development of rat HAM is under strict genetic restriction of the host strain, although HTLV-I can be transmitted equally into several strains of the rat. Neuropathological examinations show that the lesions are confined primarily to the anterior and lateral funiculi of the spinal cord. Marked demyelination with less dominant axonal damage is observed in a symmetrical fashion, and infiltration with massive foamy macrophages laden with fragmented myelins is evident. Diffuse vacuolar changes with reactive gliosis are also noted. Lymphocytic infiltration is minimal or virtually absent in the affected spinal cord. The most severe lesions are at levels of the thoracic cord and continue from the cervical to the lumbar area. The inner portion of the funiculi and central gray matter appear intact. Loss of myelin or axonal degeneration is not seen in the cerebrum, the cerebellum, or the brain stem above the level of the medulla oblongata. These histopathological features as well as clinical symptoms largely parallel findings in humans with HAM/TSP. The provirus genome is detected in the affected spinal cord by PCR but pX mRNA has not been demonstrated by in situ hybridization so far tested. Lack of lymphocytic infiltration in the affected spinal cords and no positive correlation between humoral antibodies to HTLV-I and the development of rat HAM lead us to propose that rat HAM appears to be the non-immunological demyelinating disease mediated by HTLV-I infection.


Copyright © 1993, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1243 印刷版ISSN 0001-8724 医学書院

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