这一过程即为碱基切除修复.PPT

* * Insertional activation Long latent periods, Less efficient Do not induce transformation of cells in vitro Usually are replication competent No oncogenes Tumors are usually monoclonal Provirus (LTR) is found within the vincity of a proto-oncogene (c-myc) Examples: lymphoid leukemia virus * * Transactivation HTLV-1 and 2 Like cis-activation group: replication competent, carries no oncogene, induces monoclonal leukemia Like transducing group: can immortalize cells in vitro, has no specific integration site Unique 3’ genomic structure: the X region; Encodes at least three proteins: Tax (p40), Rex (p27, p21) Tax is the focus Transactivate the viral LTR, results in a 100- to 200-fold increase in the rate of proviral transcription Transactivate cellular enhancers and promoters, including genes for IL-2, granulocyte-macrophage colony-stimulating factor (GM-CSF), c-fos, and others. * * Immunodeficiency AIDS patients have an extraordinary increased rate of developing high-grade lymphomas and Kaposi’s sarcoma (KS) Probably secondary However, Tat protein of HIV (the transactivating protein) may induce KS-like lesions in mice. * * DNA Oncovirus Papilloma virus （乳头状瘤病毒） Polyoma virus（多瘤病毒） Adenovirus Herpes virus: EB virus（疱疹病毒） Hepatitis B virus * * Mechanism of Oncogenesis Induced by DNA Oncovirus Transforming proteins 1. HPV E6 interact with P53 E7 interact with RB 2. Adenovirus E1a interact with RB E1b 3. Polyoma virus SV40（猴空泡病毒） Large T interact with RB Py virus (多瘤病毒) Large and Middle T Transcription activators 1. EB virus EBNA-2 and LMP 2. HBV p28 X protein * * Gene Map and Function of HPV ORF Function E1 Virus proliferation E2 Regulation of trans