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Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

ABSTRACT: HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on splicing patterns in CEM cells by exon microarray analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193574 | GEO | 2022/03/03

REPOSITORIES: GEO

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Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex

Project description:HTLV-1 is an onco-retrovirus that infects human T cells and causes poor prognosis leukaemia/lymphoma, ATL. The viral RNA binding protein, Rex, intervenes in host cell regulation of gene expression, splicing and translation mechanisms to promote viral particle replication, but the detailed mechanism of its function has not been elucidated. In the present study, we stably overexpressed HTLV-1 Rex in the human T-cell-derived cell line, CEM, and investigated effect of Rex on gene expression profiles in CEM cells by gene expression microarray analysis.

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Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

Project description:Human exon microarray analysis in CEM cells overexpressing HTLV-1 Rex

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Human gene expression microarray analysis in CEM cells overexpressing HTLV-1 Rex

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KDR-dependent tyrosine phosphorylation in HTLV-1 transformed cells

Project description:Human T-cell leukemia virus type 1 (HTLV-1) is linked to the development of adult T-cell leukemia (ATL) and the neuroinflammatory disease, HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax oncoprotein regulates viral gene expression and the NF-kB pathway to promote the survival of HTLV-1 infected T cells. In thsi study, we utilize a kinome-wide shRNA screen to identify the tyrosine kinase KDR/VEGFR2 as an essential survival factor of HTLV-1-transformed T cells. Inhibition of KDR induces apoptosis of Tax expressing HTLV-1-transformed cell lines and CD4+ T cells from HAM/TSP patients. Phosphoproteomics analysis of HTLV-1 transformed cells treated with a KDR inhibitor revealed inhibition of the phosphorylation of multiple receptors/cell surface proteins, ubiquitin conjugating systems, proteases, phosphatases, apoptotic regulatory factors, adhesion/extracellular matrix proteins and viral proteins. This work suggests that HTLV-1 Tax has hijacked KDR kinase activity to promote Tax stability and the proliferation and survival of HTLV-1 infected cells.

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Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.

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Thymic Epithelial Cells with Human T cell Leukemia Virus type 1 (HTLV-1) Infected T cell supernatant (CEM, CIB, C91PL)

Project description:The human T-lymphotropic virus type-1 (HTLV-1) is the cause of adult T cell leukemia/lymphoma (ATL) and HTLV-1 associated myelopathy/tropical spatic paraparesis (HAM/TSP). Both diseases have a late onset, although ATL has a medium survivor of 7.7 months after the onset despise aggressive treatment. T CD4+ cells are the main target of HTLV-1, but other cells types are known to be infected as T CD8+, CD34+ progenitor, dendritic cells and immature lymphocytes. The thymus gland is a primary lymphoid organ, in which the lymphocytes undergo differentiation, where selected T cell ultimately being exported from the organ and going to peripheral lymphoid organs. This process occurs along with immature lymphocyte migration and interaction with thymic microenvironment. Thymic epithelial cells (TECs) are the main component of the thymic stroma and are responsible for the process of intrathymic T cell maturation. This process are dependent of T cell receptor (TCR)-mediated recognition of antigenic peptide fragments presented by major histocompatibility complex (MHC) molecules in TEC and culminate in TCR repertoire formation. In this study, we show that TECs have the receptors for HTLV-1 entry and can be infected by cell-cell contact and cell-free virus. These cells change gene expression of anti-apoptosis, chemokine and adhesion molecules genes; however, there is no difference in antigen presentation molecules. Furthermore, HTLV-1 infected TECs can transmit the virus to a CD4 T cell lineage and CD4 T cells derived from peripheral blood of healthy donors after in vitro co-cultivation. Conjointly, our data points to the possibility that the human thymic epithelial cells must favor the HTLV-1 infection as a reservoir, transmitting the virus to maturing lymphocytes that cause the disease in the periphery.

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Expression data from CD4-positive HTLV-positive cell lines and from CD4-positive HTLV-negative primary cells.

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Gene expression profiling in patients infected with HTLV-1: Identification of ATL and HAM/TSP-specific genetic profiles

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