HTLV-I myelitis—Isolation of virus, genomic analysis, and infection in neural cell cultures. Takahiko SAIDA 1 , Kyoko SAIDA 1 , Masahiro FUNAUCHI 1 , Seung Kim 2 , Kazuhiko WATABE 2 , Kyoko OZAWA 1 , Etsuko NISHIGUCHI 1 , Michiko NAKAJIMA 1 , Shuichi MATSUDA 1 , Mitsuhiro OHTA 1 , Ichiro MIYAI 3 , Nobutsugu HIRONO 3 , Hiroshi NISHITANI 1 , Masakazu HATANAKA 4 1Clinical Research Center and Department of Neurology, Utano National Hospital 2Department of Neurology, University of British Columbia 3Department of Neurology, Sumitomo Hospital 4Institute for Virus Research, Kyoto University pp.773-780
Published Date 1987/10/10
DOI https://doi.org/10.11477/mf.1431905927
  • Abstract
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 In order to elucidate the pathogenetic mechanism of HTLV-I M, we have established virus producing T-cell lines from peripheral blood and CSF mononuclear cells of 25 patients with HT-LV-I M. All cell lines were positively stained with HTLV-I M sera, ATL sera, and monoclonal antibodies to HTLV-I gag proteins, P15, P19 and P24, and revealed type C viral particles by electron microscopic studies. Cytofluorographic analysis showed most of the line cells T3+, T4+, 2H4+, T8+, T11+, Tac+, (IL-2R+) Ia+ helper inducer surface markers. By the restriction map analysis, we have found two major subgroups of HTLV-I, the MT-2 type and ATK-1 type. They were almost equally distributed among the HTLV-I M patients and ATL patients. Two subgroups of HTLV-I seem to ability to cause either two diseases, ATL or HTLV-I M.

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