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[The immune response to human T-cell lymphotropic virus type 1].

Authors: E, Hanon;

[The immune response to human T-cell lymphotropic virus type 1].

Abstract

Human T-cell leukemia virus type 1 (HTLV-I) causes a chronic inflammatory syndrome named "Tropical Spastic Paraparesis: TSP/HAM". In the present study, the biological properties of HTLV-I-infected cells have been addressed in order to better understand pathogeny of this chronical disease. Analysis indicates that infected cells are potentially able to migrate into peripheral tissues and express HTLV-I Tax protein at a high frequency. The expression of the Tax protein has been associated with concomitant expression of IFN-gamma in infected cells. The production of this pro-inflammatory cytokine in the central nervous system might be responsible of the chronic inflammation processes seen in TSP/HAM patients. In this regard, the strong anti-HTLV-I cytotoxic immune response, which is present in the majority of infected individuals, might play a protective role by reducing the number infected cells in vivo.

Keywords

Inflammation, Human T-lymphotropic virus 1, Humans, Lymphocytes, HTLV-I Infections

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selected citations
These citations are derived from selected sources.
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
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