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Abstract
The level of HTLV-I expression is low in vivo. We found that recombinant interferon
(IFN)-α and β suppressed viral expression in HTLV-I-infected cells. Non-lymphoid stromal
cells also suppressed HTLV-I expression through type-I IFNs. The suppression was reversible
after isolation of infected cells from the source of IFNs, mimicking the status of
viral expression in freshly isolated ATL cells which is rapidly induced in culture.
Nevertheless, HTLV-I-infected individuals maintain acquired immune responses against
HTLV-I such as antibodies and cytotoxic T lymphocytes (CTLs), indicating the presence
of HTLV-I proteins in vivo. Analysis on Tax-specific CTLs revealed that they were
activated in HAM/TSP but unresponsive in ATL patients. We found that a subpopulation
of HTLV-I carriers at asymptomatic stage exhibited impaired Tax-specific T-cell response
and elevated HTLV-I proviral load. This combination is a feature of ATL and likely
to be an underlying risk of ATL. Collectively, HTLV-I is doubly controlled by acquired
and innate immunity; HTLV-I-specific CTLs eliminate infected cells, and IFNs suppress
viral expression. Both would contribute the reduction of viral pathogenesis, while
the efficiency of CTLs could be partial because of limited viral expression. An increase
in viral expression would activate CTLs but also accelerate inflammation. When the
viral expression is well-controlled, viral pathogenesis may not be apparent until
infected cell clones with a malignant phenotype finally emerge, which may occur earlier
without proper CTL responses. Diversity in innate and acquired immune responses among
individuals might be important determinants of disease manifestation in HTLV-I infection.
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Conference name:
15th International Conference on Human Retroviruses: HTLV and Related Viruses