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Interaction between human oncogenic retrovirus and cellular factors of infected cells.

Chiara Orlandi-2010-01-01-InsubriaSpace
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TL;DRAbstract

The purpose of this PhD thesis was to investigate the cellular and molecular interactions between oncogenic retroviruses, particularly HTLV-2 (Human T cell ymphotropic Virus 2), and host factors with potential inhibitory action on retroviral replication. Special attention was concentrated n the host factor CIITA, the HLA class II transactivator.
\nIt was previously shown in this laboratory that CIITA inhibits the transcriptional function of Tax-2 and, consequently, the replication of HTLV-2 virus in human target cells. We tested different fragments of CIITA in 293T cell line, used as a human physiologic system for functional assays with HTLV-2, for the inhibition of Tax-2. We confirm that the Nterminus of CIITA, encompassing the region 1-252, is involved in the block of the Tax-2-mediated transactivation of viral LTR promoter. We also investigated the molecular mechanism at the basis of this effect, and we an unprecedented interaction between CIITA
\nand Tax-2, that involves th

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The purpose of this PhD thesis was to investigate the cellular and molecular interactions between oncogenic retroviruses, particularly HTLV-2 (Human T cell ymphotropic Virus 2), and host factors with potential inhibitory action on retroviral replication. Special attention was concentrated n the host factor CIITA, the HLA class II transactivator.
\nIt was previously shown in this laboratory that CIITA inhibits the transcriptional function of Tax-2 and, consequently, the replication of HTLV-2 virus in human target cells. We tested different fragments of CIITA in 293T cell line, used as a human physiologic system for functional assays with HTLV-2, for the inhibition of Tax-2. We confirm that the Nterminus of CIITA, encompassing the region 1-252, is involved in the block of the Tax-2-mediated transactivation of viral LTR promoter. We also investigated the molecular mechanism at the basis of this effect, and we an unprecedented interaction between CIITA
\nand Tax-2, that involves th

Keywords

RetrovirusBiologyVirologyComputational biologyCell biologyCancer researchVirus

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