Area of Research: Basic Immunology/Virology The research of Dr. Samuel Speck focuses on Epstein-Barr virus and murine gammaherpesvirus-68, to understand the molecular mechanisms by which these viruses establish persistent, chronic infections that cannot be cleared by the body. Epstein-Barr virus (EBV) infection, which is commonly known for causing infectious mononucleosis, also is the cause of endemic Burkitt’s lymphoma, a type of cancer that primarily strikes children in the malaria belt of Africa. EBV also is associated with 30-50 percent of cases of Hodgkin’s lymphoma, a cancer that tends to occur in late adolescence. As the Georgia Research Alliance Eminent Scholar in Molecular Pathogenesis, Dr. Speck is Director of the Center for Emerging Infectious Diseases at Emory. He also is a Professor in the Division of Microbiology and Immunology of the Yerkes National Primate Research Center of Emory. Prior to his 1999 arrival at Emory, he was a Professor in the Department of Pathology at Washington University School of Medicine. Dr. Speck received his Ph.D. in biochemistry and molecular biology from Northwestern University. Research
Dr. Speck was recently recruited from The Washington University School of Medicine and officially came on board here at Emory in June 2001. He is a Georgia Research Alliance Eminent Scholar and Endowed Professor, and Director, Center for Emerging Infectious Diseases, Department of Microbiology & Immunology, Emory University School of Medicine. The research in Dr. Speck’s lab focuses on 2 gamma-herpesviruses, Epstein-Barr virus (EBV) and murine gamma-herpesvirus 68 (HV68). A major property of all herpesviruses is their ability to persist for life in the infected individual. The gamma-herpesviruses are known to latently infect either B or T lymphocytes, and to be associated with the development of lymphoma and lymphoproliferative diseases. Their major interests are to understand: (i) how these viruses regulate viral gene expression during latency; (ii) how they modulate and avoid the host immune response; and (iii) how they switch from a latent infection to replication of the viral genome (referred to as reactivation), a process that is essential for propagation of these viruses to uninfected individuals. Their research on EBV focuses on tissue culture models that recapitulate the various EBV genetic programs. The information gained from these studies is then employed to address the behavior of EBV in infected individuals. However, because there are no small animal models for studying EBV pathogenesis, they use HV68 infection of mice to address specific issues of the host response to gamma-herpesvirus infection. HV68 infection of mice causes several different chronic diseases in immunocompromised mice, including a severe vasculitis that affects the great elastic arteries and lymphoproliferative disease. Speck and his team are currently identifying HV68 genes involved in establishing and maintaining viral latency, as well as those involved in the development of chronic disease. In addition, they are actively characterizing the host response to viral infection to address how viral latency and persistent infection is controlled.
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