Summary: | <p>Abstract</p> <p>Human T-lymphotropic virus type-1 (HTLV-1) is a complex retrovirus that causes adult T-cell leukemia/lymphoma (ATL) and is implicated in a variety of lymphocyte-mediated disorders. HTLV-1 pX ORF II encodes two proteins, p13<sup>II </sup>and p30<sup>II </sup>whose roles are beginning to be defined in the virus life cycle. Previous studies indicate the importance of these viral proteins in the ability of the virus to maintain viral loads and persist in an animal model of HTLV-1 infection. Intriguing new studies indicate that p30<sup>II </sup>is a multifunctional regulator that differentially modulates CREB and Tax-responsive element-mediated transcription through its interaction with CREB-binding protein (CBP)/p300 and specifically binds and represses <it>tax/rex </it>mRNA nuclear export. A new study characterized the role of p30<sup>II </sup>in regulation of cellular gene expression using comprehensive human gene arrays. Interestingly, p30<sup>II </sup>is an overall repressor of cellular gene expression, while selectively favoring the expression of regulatory gene pathways important to T lymphocytes. These new findings suggest that HTLV-1, which is associated with lymphoproliferative diseases, uses p30<sup>II </sup>to selectively repress cellular and viral gene expression to favor the survival of cellular targets ultimately resulting in leukemogenesis.</p>
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