
doi: 10.2741/1401
pmid: 15353292
HTLV-1 is the etiological agent of the fatal disease adult T-cell leukemia. The virus encodes many proteins including several accessory proteins, p12I, p13II, p27I, and p30II, whose roles have recently begun to be elucidated. These accessory proteins are important in T-cell activation, transcriptional regulation, viral persistence, and virus assembly. The viral oncogene Tax is thought to be largely responsible for tumorigenesis, although the precise mechanisms underlying transformation are not completely understood. Tax has a profound impact on transcription, cell growth regulation, genomic stability and apoptosis. This review will provide possible contributions of the accessory proteins to transformation as well as highlight the alterations of the above-mentioned cellular events by Tax. Animal models of both Tax and the accessory proteins are also included based on the essential information on the transformation process in vivo that they provide.
Gene Expression Regulation, Viral, Human T-lymphotropic virus 1, Leukemia, T-Cell, DNA Repair, Transcription, Genetic, Cell Cycle, Mitosis, Apoptosis, Gene Products, tax, Oncogene Proteins, Viral, Cell Transformation, Viral, Lymphocyte Activation, Virus Replication, Disease Models, Animal, Cell Transformation, Neoplastic, Animals, Humans, Viral Regulatory and Accessory Proteins, Cell Proliferation
Gene Expression Regulation, Viral, Human T-lymphotropic virus 1, Leukemia, T-Cell, DNA Repair, Transcription, Genetic, Cell Cycle, Mitosis, Apoptosis, Gene Products, tax, Oncogene Proteins, Viral, Cell Transformation, Viral, Lymphocyte Activation, Virus Replication, Disease Models, Animal, Cell Transformation, Neoplastic, Animals, Humans, Viral Regulatory and Accessory Proteins, Cell Proliferation
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