Epstein-Barr Virus Alteration of Lymphocyte Growth |
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| Air date: | Wednesday, May 14, 2008, 3:00:00 PM |
| Category: | Wednesday Afternoon Lectures |
| Runtime: | 75 minutes |
| NLM Title: | Epstein-Barr virus alteration of lymphocyte growth [electronic resource] / Elliott Kieff. |
| Series: | NIH director's Wednesday afternoon lecture series |
| Author: | Kieff, Elliott D. National Institutes of Health (U.S.) |
| Publisher: | [Bethesda, Md. : National Institutes of Health, 2008] |
| Other Title(s): | NIH director's Wednesday afternoon lecture series |
| Abstract: | (CIT): Human viruses are responsible for about 20% of human malignancies worldwide and offer unique opportunities for early diagnosis, prevention, and therapeutic intervention. Our experiments began with the study of the fundamental mechanisms by which Epstein-Barr Virus (EPV), an important causative agent of lymphomas, Hodgkin's Disease and Naso-pharyngeal carcinoma, uniquely and efficiently causes the uncontrolled proliferation and survival of normal human B lymphocytes. We have discovered that the virus uses only five genes to cause B cell proliferation. These genes encode nuclear proteins that usurp control over Notch regulated cell promoters, including the c-myc promoter, and an integral membrane protein that constitutively activates CD40 signaling pathways. We are currently investigating the genetics and biochemistry of the molecular and sub-molecular processes through which the viral proteins effect changes in cell signal transduction, transcription, growth, and survival so as to validate targets that can be used in assays to identify chemical inhibitors. EBV is unique among human viruses in inducing continuous proliferation of B lymphocytes, the important host cell for EBV latency. In B lymphocytes, EBV encodes nuclear antigen (EBNA) and integral membrane (LMP) proteins, which induce cell cycle transit and lymphoblast proliferation. In humans with normal T cell function, immune T lymphocytes emerge in response to peptides from the EBNAs and LMPs, which are presented in the context of Class I and II MHC molecules on cell surfaces. Immune T cells kill and enforce tight control of EBV infected lymphocytes. Ongoing projects in our lab involve: (1) Elucidation of the molecular and sub-molecular pathways by which Notch and viral proteins regulate the c-myc promoter. Structural studies of a key viral and cellular interaction site. (2) Elucidation of the molecular and sub-molecular pathways by which CD40 and a viral protein co-stimulate cell growth and survival. (3) Proteinomic and cell genetic screens for novel genes in the CD40 and viral protein NF-kB, Junk, and p38 pathways. (4) Sub-molecular mechanisms by which a viral protein permits episome replication and maintenance. |
| Subjects: | B-Lymphocytes--virology Cell Proliferation Herpesvirus 4, Human Neoplasms--virology |
| Publication Types: | Government Publications Lectures |
| Download: | Download
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| NLM Classification: | QW 165.5.H3 |
| NLM ID: | 101475716 |
| CIT File ID: | 14496 |
| CIT Live ID: | 6223 |
| Permanent link: | http://videocast.nih.gov/launch.asp?14496 |
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Enhanced Audio Podcast | 1:03:40 |
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Enhanced Video Podcast | 1:03:40 | |