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Virology |
Basic Research Laboratory, Virus Tumor Biology Section, National Cancer Institute, Bethesda, Maryland 20892 [C. A. P-M., M. R., P. C., J. D., C. G., J. N. B.]; Unite d’Epidemiologie et Physiopathologie des Virus Oncogenes, Batiment SIDA-Retrovirus, Institut Pasteur, 75724, Cedex 15, Paris, France [R. M., A. G.]; and Advanced Technology Center, National Institutes of Health, Gaithersburg, Maryland [C. W.]
Human T-cell leukemia virus type I (HTLV-I) is the etiologic agent for adult T-cell leukemia and the neurological disorder tropical spastic paraparesis/HTLV-I-associated myelopathy. CD4+ T lymphocytes, the primary hosts for HTLV-I, undergo a series of changes that lead to T-cell activation, immortalization, and transformation. To gain insight into the genetic differences between activated and HTLV-I-infected lymphocytes, we performed Affymetrix GeneChip analysis of activated and HTLV-I-infected cells. Using the Hu6800 GeneChip, we identified 
763 genes that had differentially regulated expression in at least three of five HTLV-I cell lines. Classification of these genes into functional groups including cellular receptors, kinases, phosphatases, cytokines, signal proteins, and transcription factors provides insight into genes and pathways that are differentially regulated during HTLV-I transformation.
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