Edward I. Shaw
Microbiology and Molecular Genetics
B.S., 1989, Georgia Southwestern College
Ph.D., 1997. University of South Alabama College of Medicine (D. O. Wood, mentor)
Post-doc, 1997-2000, Rocky Mountain Laboratories, NIH (Ted Hackstadt, mentor)
Senior Service Fellow/Microbiologist, 2000-2004, Centers for Disease Control (Atlanta)
Assistant Professor, 2005-2011, OSU Dept. of Microbiology and Molecular Genetics
Associate Professor, 2011-present, OSU Dept. of Microbiology and Molecular Genetics
My lab is interested in the molecular interactions between obligate-intracellular bacterial pathogens and their eukaryotic host-cell. I have worked with Rickettsiae, Chlamydiae, and Coxiellae species during my career.Our current research is focused on the obligate-intracellular bacteria, Coxiella burnetii. C. burnetii is the etiologic agent of Q fever and chronic diseases such as endocarditis, hepatitis, and chronic fatigue. The acute form is typically a self-limiting flu-like illness that ranges from sub-clinical to severe. Within the subset of chronic diseases, the most common clinical result is valvular endocarditis (Q fever endocarditis). While data on the number of Q fever endocarditis cases in the U.S. are unavailable, studies in Europe have implicated C. burnetii as a major cause in non-culturable endocarditis cases.Reservoirs for C. burnetii include animal populations (particularly ruminants) which develop chronic infections and shed environmentally-stable infectious particles that can infect humans by inhalation.As such, this zoonotic pathogen poses a significant risk to persons involved in the cattle, sheep, and goat industries.In addition, because of its potential for efficient aerosol spread and its capability of causing both acute and chronic severe disease, it has been designated a Select Agent and potential bioterror threat by the CDC.
C. burnetii is an obligate intracellular bacterial pathogen that is typically acquired through aerosol exposure. Initial infection occurs in lung alveolar macrophages and is followed by a bi-phasic life cycle involving two stages, or variants: first is the environmentally stable small cell variant (SCV), and second is the metabolically active, and replicative, large cell variant (LCV). While both are infectious in cell culture systems, SCVs are thought to be the primary cause of infections in nature. After infecting the host cell, C. burnetii replicates in parasitophorous vacuoles that retain many of the features of mature phagolysosomes.Many pathogenic intracellular bacterial species, including Coxiella, direct their own phagocytosis, use host cell materials (i.e. amino acids, nucleotides, etc.) to their advantage and attempt to evade host immune responses.The molecular mechanisms used by C. burnetii to parasitize their host cells are largely unknown.The genome of several C. burnetii strains has been sequenced and is beginning to reveal clues towards understanding the mechanisms used by this unique pathogen to survive within the harsh environment of the host cell phagosome and cause disease. The long term goal of our research is to elucidate molecular interaction pathways between C. burnetii and its host cell during the infectious cycle.
Research efforts in my lab are currently centered on:
(1) Characterizing the C. burnetii type IV secretion system, a known virulence mechanisms in bacteria, throughout the C. burnetii life-cycle.
(2) Looking at host cell gene expression/cellular pathway changes driven by C. burnetii protein synthesis throughout infection.This includes looking at changes in host signaling pathways driven by C. burnetii.
Understanding bacterial and host factors which may be involved in the invasion, intracellular trafficking, host immune-avoidance, and subsequent replication of C. burnetii in this hostile environment may lead to novel diagnostic, detection, or intervention strategies.