Dr. Everly received his B.A. in Biology in 1991 from William Jewell College in Liberty, MO. He received his Ph.D. in Cell Biology and Biophysics, and Molecular Biology and Biochemistry from the University of Missouri-Kansas City in 1998 studying herpes simplex virus virion host shutoff. He continued his studies at UMKC from 1998-2001 as a postdoctoral fellow. In 2001 he joined the laboratory of Nancy Raab-Traub in the Linberger Comprehensive Cancer Center at the University of North Carolina-Chapel Hill to study tumor virology and Epstein-Barr virus. He was appointed Research Assistant Professor in 2006 in the department of Microbiology and Immunology at UNC. Dr. Everly joined the Department of Microbiology and Immunology as an Assistant Professor at Rosalind Franklin University of Medicine and Science in August of 2007.
Epstein-Barr virus (EBV) is a ubiquitous infectious agent that infects greater than 90% of the world’s population and is the etiologic agent of infectious mononucleosis. EBV is also a DNA tumor virus that is associated with a number of human malignancies and efficiently transforms B-lymphocytes. Burkitt’s lymphoma and nasopharyngeal carcinoma are highly associated with EBV, while some types of Hodgkin disease and some gastric cancers contain EBV. EBV-infected B-cell lymphomas are a significant complication of immunosuppressed conditions, including post-transplant and AIDS-associated lymphomas. Our laboratory studies the cellular signaling pathways that are important for different aspects of EBV biology. First, in viral oncogenesis, we are interested in latent membrane protein 1 (LMP1) and its role in EBV-associated cancers. LMP1, termed the EBV oncogene, is expressed in most EBV-associated cancers, is essential for B-cell transformation, and is sufficient for rodent fibroblast transformation. Our studies using rodent fibroblast transformation have yielded new insights into the mechanisms of transformation by LMP1, including regulation of cell cycle proteins and definition of pathways required for transformation. A second interest in the lab concerns signaling cascades induced by EBV infection. Binding of viruses to their cellular receptors not only gives the virus a point of entry into the infected cell, but also initiates signaling pathways important for the establishment of an environment favorable for viral infection and survival of the infected cell. Understanding signaling pathways and factors induced by EBV infection will define new areas of viral pathogenesis. Each newly defined mechanism will illuminate new potential points of intervention in viral infection and oncogenesis.
Talaty, P., Emery, A, and Everly D.N., “Characterization of the Latent Membrane Protein 1 Signaling Complex of Epstein-Barr Virus in the Membrane of Mammalian Cells with Bimolecular Fluorescence Complementation.” Virology Journal, Aug 24;8(1):414, 2011.
Everly, D.N., Jr., Sharma-Walia, N, Sadagopan, S., and Chandran, B, “Herpesviruses and Cancer” in Virus-Associated Cancers by Erle Robertson.
Everly, D.N., Jr., Mainou, B. A. and Raab-Traub, N., “Transcriptional Downregulation of p27KIP1 through Regulation of E2F Function during LMP1-Mediated Transformation,” J. Virology 83:12671-12679, 2009.
Everly, D.N., Jr., Mainou B.A., and Raab-Traub N., “The Id proteins contribute to the growth of Rodent Fibroblasts During LMP1-Mediated Transformation”, Virology 376: 258-269, 2008.
Mainou B.A., Everly, D.N., Jr., and Raab-Traub N., Unique Signaling Properties of CTAR1 in LMP1-Mediated Transformation,” J. Virology 81: 9680-9692, 2007.
Feng, P., Everly, D.N., Jr., and Read, G.S., “mRNA Decay During Herpes Simplex Virus (HSV) Infections: Protein-Protein Interactions Involving the HSV Virion Host Shutoff Protein and Translation Factors eIF4H and eIF4A.,” J. Virology, 79: 9651-9664, 2005.
Mainou, B.A., Everly, D.N., Jr., and Raab-Traub, N., “Epstein-Barr Virus Latent Membrane Protein 1 CTAR1 Mediates Rodent and Human Fibroblast Transformation Through Activation of PI3K,” Oncogene, 24:6917-24, 2005.
Everly, D.N., Jr., Mainou, B.A., and Raab-Traub, N., “Induction of Id1 and Id3 by Latent Membrane Protein 1 of Epstein-Barr Virus and Regulation of p27/KIP and Cyclin Dependent Kinase 2 in Rodent Fibroblast Transformation,” J. Virology, 78:13470-13478, 2004.
Everly, D.N., Jr., Kusano, S., and Raab-Traub, N., “Accumulation of Cytoplasmic β-Catenin and Nuclear Glycogen Synthase Kinase 3β in Epstein-Barr Virus Infected Cells,” J. Virology, 78:11648-11655, 2004.
Everly, D.N., Jr., Feng, P., Mian, I.S., and Read, G.S., “mRNA Degradation by the Virion Host Shutoff (VHS) Protein of Herpes Simplex Virus: Genetic and Biochemical Evidence that VHS is a Nuclease,” J. Virology, 76:8560-71, 2002.
Feng, P., Everly, D.N., Jr., and Read, G.S., “mRNA Decay During Herpesvirus Infections: Interaction Between a Putative Viral Nuclease and a Cellular Translation Factor,” J. Virology, 75:10272-80, 2001.
Everly, D.N., Jr. and Read, G.S., “Site-Directed Mutagenesis of the Virion Host Shutoff Gene (UL41) of Herpes Simplex Virus (HSV): Analysis of Functional Differences between HSV type 1 (HSV-1) and HSV-2 Alleles,” J. Virology, 73:9117-9129, 1999.
Everly, D.N., Jr. and Read, G.S., “Mutational Analysis of the Virion Host Shutoff Gene (UL41) of Herpes Simplex Virus (HSV): Characterization of HSV type 1 (HSV-1)/HSV-2 Chimeras,” J. Virology 71:7157-7166, 1997.
Pak, A.S., Everly, D.N., Jr. Knight, K., and Read, G.S., “The Virion Host Shutoff Protein of Herpes Simplex Virus Inhibits Reporter Gene Expression in the Absence of other Viral Gene Products,” Virology 211:491-506, 1995.