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Richard M. Longnecker, PhDCongressman John Edward Porter Professor
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To visit the Longnecker Lab website at click here.
Diseases in humans caused by EBV, being primarily of lymphoid or epithelial origin, reflect the cell types that EBV infects. The most notable lymphoid disease, infectious mononucleosis, is a self limiting lymphoproliferative disease in normal adolescents which occurs upon primary infection. EBV is also associated with hemopoietic cancers such as African Burkitt's lymphoma, Hodgkin’s and adult T-cell leukemia. The two notable epithelial diseases associated with EBV infection are nasopharyngeal cancer, a malignancy endemic to southern China; and oral hairy leukoplakia, an epithelial hyperplasia of the lingual squamous epithelium in AIDS patients.
The Longnecker laboratory focuses on several aspects of EBV pathogenesis. First, the laboratory is interested in transformation. Specifically, research is being conducted to understand the molecular basis of the ability of EBV to transform and provide anti-apoptotic signals to primary B lymphocytes. These studies are particularly important because of the association of EBV with a human cancer. Second, the laboratory is interested in understanding the ability of the virus to persist and remain latent in human host. In this regard, the laboratory is developing animal models for EBV latent infections. These studies will be important in understanding the unique ability of viruses to remain latent in the human host and disease syndromes associated with these latent infections. Finally, the laboratory is investigating viral entry, assembly, and cellular genes that are required for viral entry. Ultimately we these studies will provide insight for the development of novel therapeutics for the treatment of EBV related malignancies, an understanding of the virus life cycle, and an understanding of signal transduction and cell growth regulation in lymphocytes.
Mullen M, Haan KM, Longnecker R, and Jardetzky T. Crystal Structure of the Epstein-Barr Virus gp42 Glycoprotein Bound to HLA-DR1. Molecular Cell 2002; 9:375-85
Cooper L, and Longnecker R. Inhibition of Host Kinase Activity Altered by the LMP2A Signalosome - A Therapeutic Target for Epstein-Barr Virus Latency and Associated Disease. Antiviral Research 2002; 219-231.
Portis T, and Longnecker R. EBV LMP2A Interferes with Global Transcription Factor Regulation when Expressed During B Cell Development. Journal of Virology 2003:77:105-114.
Ikeda A, Caldwell R, Longnecker R, and Ikeda M. Itchy, a Nedd4 Ubiquitin Ligase, Downregulates LMP2A Activity in B Cell Signaling. Journal of Virology 2003:77:5529-5534.
McShane M, Haan KM, Mullen M, Jardetzky T, Longnecker R. Mutational Analysis of the HLA Class II Interaction with the Epstein-Barr Virus (EBV) Glycoprotein 42 (gp42). Journal of Virology 2003;77:7655-7662.
Spear PG, Longnecker R. Herpesvirus Entry: An Update. Journal of Virology, 2003;77:10179-10185.
Katzman RB, Longnecker R. Cholesterol Dependent Entry of Epstein-Barr Virus into B lymphocytes. Journal of General Virology, 2003;84:2987-2992
Portis T, Longnecker R. Epstein-Barr Virus (EBV) Induces Alterations in Gene Transcription Similar to Those Observed in Reed-Sternberg Cells of Hodgkin's Lymphoma. Blood 2003,102:4166-4178.
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View Publications by Richard Longnecker listed in the National Library of Medicine (PubMed). |
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