1995 Fiscal Year Final Research Report Summary
Spontaneous inhibition of HTL V-I expression in the peripheral blood
| Project/Area Number |
06670333
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Tokyo Medical and Dental University (1995)
Kumamoto University (1994) |
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Principal Investigator |
KANNAGI Mari Tokyo Medical and Dental University・Medical Research Division, Professor, 医学系研究科, 教授 (80202034)
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| Project Period (FY) |
1994 – 1995
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| Keywords | HTLV-I / Antigen expression / ATL / Plasma factor. |
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| Research Abstract |
Human T-cell leukemia virus type-I (HTLV-I) is associated with adult T cell leukemia (ATL) and HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP). HTLV-I tax is one of the main target antigens recognized by HTLV-I-specific cytotoxic T lymphocytes (CTL). This is advantageous for the host, because cytolysis probably occurs at an early stage of leukemogenesis.
Immediate detection of CTL activity in the PBMC is unusual, because virusspecific CTL activity resulting from prior infection can be detected generally only after in vitro restimulation. A similar phenomenon has been noted in humanimmunodeficiency viruus infection, which is believed to reflect active immune stimulation in vivo. The level of HTLV-I expression is elevated in the peripheral blood of HAM/TSP patients. However, the level of HTLV-I gene expression could be spontaneously elevated in vitro. Fresh leukemia cells of ATL patients only marginally expressed HTLV-I mRNA,but showed a significant induction of HTLV-I mRNA and antigens following in vitro incubation in vitro. Such induction was observed in the PBMC of asymptomatic HTLV-I carriers and HAM/TSP patients. This suppression of HTLV-I expression, presumably mediated by a plasma factor and commonly observed in HTLV-I-infected individuals, could be one reason for the persistence of HTLV-I-infection.
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