Human T-cell leukemia virus type 1: Transition from latent infection to pathogenic progression and implications for molecular therapy

Yulia Tabakin-Fix, Inbal Azran-Shaish, Yana Schavinsky-Khrapunsky, Rachel Chamias, Lilach Gohari, Mahmoud Huleihel, Min Li-Weber, Mordechai Aboud

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations

Abstract

HTLV-1 is etiologically implicated with adult T-cell leukemia (ATL) and tropical spastic paraparesis/HTLV-1 associated myelopathy (TSP/HAM). Neither of them is curable by presently known therapy. Therefore, both disorders are waiting for novel therapeutic approaches. Developing such approaches requires comprehensive insight into the viral and cellular factors involved in the genesis of these diseases. It is widely accepted that the viral Tax protein plays a key role in initiating the process leading to ATL, as well as in the pathogenesis of TSP/HAM. Therefore, its various activities are attractive targets for novel molecular or/and immunological therapies. This review describes the effects of Tax that confer its oncogenic potential. These effects require a sufficiently high level of Tax protein, whereas shortly after human infection, the virus enters into a latent state in which no or very low viral gene expression and Tax protein can be detected in the infected cells of the virus carriers. This implies that the dormant virus must be activated in order to elevate Tax protein to its effective level. We review here our and others' data suggesting that this activation can be triggered by stress-inducing environmental agents and discuss the mechanism of this activation. In addition, we discuss the pathogenic progression following this virus activation and finally we present perspectives for molecular therapeutic approach for HTLV-1 related clinical disorders.

Original languageEnglish
Pages (from-to)101-113
Number of pages13
JournalCurrent Cancer Therapy Reviews
Volume2
Issue number2
DOIs
StatePublished - 1 May 2006

Keywords

  • ATL
  • Apoptosis
  • Genetic instability
  • HTLV-1
  • TSP/HAM
  • Tax

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