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Human T‐lymphotropic virus type I‐associated myelopathy and tax gene expression in CD4 + T lymphocytes
Author(s) -
Moritoyo Takashi,
Reinhart Todd A.,
Haase Ashley T.,
Moritoyo Hiroyoko,
Izumo Shuji,
Osame Mitsuhiro,
Sato Eiichi
Publication year - 1996
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410400114
Subject(s) - tropical spastic paraparesis , cytotoxic t cell , myelopathy , human t lymphotropic virus , human t lymphotropic virus 1 , virus , cd8 , immunology , biology , inflammation , t cell leukemia , virology , spinal cord , pathology , medicine , antigen , biochemistry , neuroscience , in vitro
Infection by human T‐lymphotropic virus type I (HTLV‐I) is associated with adult T‐cell leukemia and a slowly progressive disease of the central nervous system (CNS), HTLV‐I‐associated myelopathy/tropical spastic paraparesis, characterized pathologically by inflammation and white matter degeneration in the spinal cord. One of the explanations for the tissue destruction is that HTLV‐I infects cells in the CNS, or HTLV‐I‐infected CD4 + T lymphocytes enter the CNS, and this drives local expansion of virus‐specific CD8 + cytotoxic T lymphocytes, which along with cytokines cause the pathological changes. Because both in the circulation and in the cerebrospinal fluid, CD8 + cytotoxic T lymphocytes are primarily reactive to the product of the HTLV‐I tax gene, we sought evidence of expression of this gene within cells in the inflammatory lesions. After using double‐label in situ hybridization techniques, we now report definitive localization of HTLV‐I tax gene expression in CD4 + T lymphocytes in areas of inflammation and white matter destruction. These findings lend support to a hypothetical scheme of neuropathogenesis in which HTLV‐I tax gene expression provokes and sustains an immunopathological process that progressively destroys myelin and axons in the spinal cord.