Molecular and cellular events at the onset of the lymphoproliferative process induced by HTLV-I (human T-cell leukemia virus, type I).
The human retrovirology opened its first chapter, 10 years ago, with the isolation and characterization of HTLV-I (Human T-cell leukemia virus, type I), a type C retrovirus, which was found to be etiologically linked first to adult T-cell leukemia and second to neurological disorders. Epidemiological data have indeed shown that patients who developed these diseases represent a small percentage of HTLV-I infected individuals living in restricted geographical areas. Experiments performed at molecular and cellular levels have revealed that HTLV-I plays an essential role in the initiation of the lymphoproliferative process. Indeed, viral particles deliver a mitogenic signal to human resting T lymphocytes. After proviral integration, two regulatory proteins--Tax and Rex--are controlling the replicative cycle of HTLV-I. The Tax protein trans-activates the proviral transcription and the Rex protein is essential in the synthesis of viral structural proteins. Furthermore, the Tax protein induces the transcription of several cellular genes involved in T-cell activation and proliferation. Studies are now aimed at identifying HTLV-I target cells among precursors of the T cell lineage and at unravelling the role of HTLV-I in the secondary events leading to leukemogenesis.
Gazzolo
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L
Laboratoire d'immuno-virologie moléculaire et cellulaire, UMR30-CNRS/UCBL, faculté de médecine Alexis-Carrel, Lyon, France.
Duc Dodon
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M
D016370:Gene Products, rex / Q000378:metabolism; D016356:Gene Products, tax / Q000378:metabolism; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism*; D006801:Humans; D008232:Lymphoproliferative Disorders / Q000378:metabolism / Q000382:microbiology*; D014759:Viral Envelope Proteins / Q000378:metabolism
D016370:Gene Products, rex; D016356:Gene Products, tax; D014759:Viral Envelope Proteins