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RAPID SYNCYTIUM FORMATION BETWEEN HUMAN T‐CELL LEUKAEMIA VIRUS TYPE‐I (HTLV‐I)‐INFECTED T‐CELLS AND HUMAN NERVOUS SYSTEM CELLS: A POSSIBLE IMPLICATION FOR TROPICAL SPASTIC PARAPARESIS/HTLV‐I ASSOCIATED MYELOPATHY
Author(s) -
MORVAKNIN NIRIT,
TURGEMAN HAVA,
TORGEMAN AMRAM,
WOLFSON MARINA,
HULEIHEL MAHMOUD,
ABOUD MORDECHAI
Publication year - 1998
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1006/cbir.1998.0241
Subject(s) - tropical spastic paraparesis , syncytium , cytotoxic t cell , biology , virology , virus , cell culture , human t lymphotropic virus 1 , astrocyte , cell fusion , cytopathic effect , blood–brain barrier , immunology , myelopathy , central nervous system , t cell leukemia , in vitro , spinal cord , genetics , neuroscience , biochemistry
Tropical spastic paraparesis/HTLV‐I associated myelopathy (TSP/HAM), is characterized by infiltration of human T cell leukaemia virus type‐I (HTLV‐I)‐infected T‐cells, anti‐HTLV‐I cytotoxic T cells and macrophages into the patients’ cerebrospinal fluid and by intrathecally formed anti‐HTLV‐I antibodies. This implies that the disease involves a breakdown of the blood—brain barrier. Since astrocytes play a central role in establishing this barrier, the authors investigated the hypothesis that the HTLV‐I infected T cells disrupt this barrier by damaging the astrocytes. The present study revealed the HTLV‐I‐producing T cells conferred a severe cytopatic effect upon monolayers of astrocytoma cell line in co‐cultures. Following co‐cultivation, HTLV‐I DNA and proteins appeared in the monolayer cells, but after reaching a peak their level gradually declined. This appearance of the viral components was proved to result from a fusion of the astrocytic cells with the virus‐producing T cells, whereas their subsequent decline reflected the destruction of the resulting syncytia. This fusion could be specifically blocked by anti HTLV‐I Env antibodies, indicating that it was mediated by the viral Env proteins expressed on the surface of the virus‐producing cells. Similar fusion was observed between the HTLV‐I‐producing cells and certain other human nervous system cell lines. If such fusion of HTLV‐I‐infected T cells occurs also with astrocytes and other nervous system cells in TSP/HAM patients, it may account, at least partially, for the blood—brain barrier breakdown and some of the neural lesions in this syndrome.