William Shafer, PhD
William Shafer received his PhD degree in Microbiology from Kansas State University in 1979 where he studied the genetics of enterotoxin synthesis by Staphylococcus aureus. After postdoctoral studies with P.F. Sparling at the University of North Carolina where he studied the genetics of antibiotic resistance expressed by Neisseria gonorrhoeae, he moved to Emory University School of Medicine where he now Full Professor. He is also a Senior Research Career Scientist at the Atlanta VA Medical Center. He has been continually funded by the NIH and VA since 1984, has published over 115 manuscripts, serves on multiple Editorial Boards and served on several NIH, VA and international study sections.
Edgar Sherman, BS
Edgar Sherman received his BS from The University of Texas at San Antonio (UTSA) in 2014. Edgar developed a strong interest in microbial genetics following two research internships where he investigated the role of mitochondrial gene function in eukaryotic respiration at The University of Texas at Austin and studied how protein turnover affects aging in rodents at The University of Texas Health Science Center in San Antonio. At UTSA, Edgar’s research focused on mechanisms of biofilm formation in the nosocomial pathogen Acinetobacter baumannii by targeting genes involved in bacterial cell signaling. After graduating, Edgar was accepted into the Microbiology and Molecular Genetics (MMG) program at Emory University where his research interest in antimicrobial resistance led him to join Dr. David Weiss’ lab and focus on studying antibiotic resistance mechanisms in Multi-drug resistant Gram-Negative pathogens. Specifically, Edgar’s research focuses on understanding the underlying genetic pathways facilitating resistance to aminoglycosides, an important class of antibiotics, in A. baumannii and how these mechanisms lead to treatment failure in a patient. Under the Antimicrobial Resistance and Therapeutic Discovery Training Program, Edgar seeks to characterize novel resistance mechanisms to ultimately improve patient outcome and expand our understanding on how bacteria evolve to combat our clinical therapeutics.
David S. Weiss, PhD
David S. Weiss is an Associate Professor in the Division of Infectious Diseases and Co-Director of the Emory Antibiotic Resistance Center. His lab's research is focused on understanding mechanisms of antibiotic resistance employed by Gram-negative nosocomial pathogens such as Acinetobacter baumannii and Enterobacter cloacae. His lab has identified and mechanistically characterized several novel genes that contribute to resistance to the last-line, cationic polymyxin antibiotics in diverse bacteria. Furthermore, this research has shown that the development of polymyxin resistance in treated patients leads to cross-resistance to cationic antimicrobial peptides of the host innate immune system. Thus, polymyxin treatment may select for bacterial strains with increased virulence. In addition to how antibiotics may alter bacterial susceptibility to the immune system, his lab is very interested in exploring the causes of unexplained treatment failures in which antibiotic therapy is ineffective despite bacterial strains appearing to be susceptible to a given antibiotic.
Sarah Anderson, BS
Sarah Anderson received her BS in 2013 from the University of North Carolina, where she double majored in biology and chemistry. As an undergraduate, Sarah conducted research projects on gene regulation in Drosophila melanogaster, and on innate immune responses to influenza infection. Following graduation, she was awarded an APHL/CDC Emerging Infectious Diseases (EID) Fellowship to conduct research at the Wadsworth Center in the New York State Department of Health. There she developed a diagnostic assay to detect fluoroquinolone-resistant Mycobacterium tuberculosis, and worked on a basic research project studying conjugation in Mycobacterium smegmatis. Sarah enrolled in the Microbiology and Molecular Genetics program at Emory University in 2014. Her interests in antibiotic resistance, bacterial genetics, and pathogenesis led her to join the laboratory of Dr. Philip Rather. Sarah’s current research in the Rather lab focuses on understanding the mechanisms regulating phase variation and intrinsic antimicrobial resistance in Acinetobacter baumannii. By participating in the Antimicrobial Resistance and Therapeutic Discovery Training program, Sarah hopes to expand her training outside of the laboratory by presenting her work at conferences and networking with scientists both inside and outside academia.
Philip N. Rather, PhD
Philip N. Rather is a Professor in the Department of Microbiology and Immunology. His lab studies the mechanisms of virulence and intrinsic antibiotic resistance in the nosocomial pathogen Acinetobacter baumannii. A novel regulatory switch has been identified in A. baumannii that results in the interconversion between two phenotypically distinct cell types distinguished by their opaque or translucent colony opacity phenotype. The opaque variant is virulent and exhibits higher levels of resistance to cationic antimicrobials. The regulatory mechanism controlling this interconversion is under investigation as well as identifying the differentially expressed genes that confer increased virulence and resistance to cationic antimicrobials. A second area of focus is the regulation of intrinsic beta-lactam resistance in A. baumannii. For this area of study, a link between cell division and chromosomally mediated beta-lactam resistance has been identified and is being characterized.
Kara Phipps, BS
Kara Phipps graduated in 2014 with a BS in Biology from Southwest Baptist University. While at SBU, Kara developed a strong interest in the study and control of infectious diseases and participated in undergraduate research. Her studies focused on the relationship between DNA damage responses to fluoroquinolone treatment and biofilm formation and motility in Pseudomonas aeruginosa. Upon entering the Microbiology and Molecular Genetics program at Emory University, Kara joined the laboratory of Anice Lowen to study the factors which impact gene reassortment and diversification of influenza viruses. Kara particularly seeks to identify mechanisms which impact reassortment and viral diversification following transfer of influenza viruses to a non-native host species. With the opportunities and support provided by the Antimicrobial Resistance and Therapeutic Discovery Training Program, Kara hopes to further current knowledge of the basic mechanisms by which influenza viruses evolve to allow escape of current antiviral treatments and vaccine-induced immunity.
Dr. Lowen is an Assistant Professor in the Department of Microbiology and Immunology, Emory University School of Medicine. She obtained her PhD from the University of Glasgow, UK, and carried out postdoctoral training at Mount Sinai School of Medicine in New York, NY.
Despite its clear importance to the epidemiology of influenza, the process by which human influenza viruses travel from one individual to another is not well understood. Prior to the zoonotic outbreak of H5N1 influenza viruses in Southeast Asia, it was generally assumed that if an influenza virus could productively infect a given host species, that virus would also transmit among individuals of that species. The lack of transmission of H5N1 influenza viruses among humans and other mammals has shown that, on the contrary, viral growth is not the only prerequisite for transmission. Research over the past six years has revealed that viral, host and environmental factors each play a role in determining the efficiency with which an influenza virus transmits. We previously showed, for example, that ambient conditions of humidity and temperature have a strong impact on the efficiency of transmission, that host-specific adaptive changes in the viral polymerase can alter transmission efficiency, and that host immunity resulting from either vaccination or natural infection limits transmission to varying degrees. Despite such progress, an in-depth understanding of transmission remains a high priority in the influenza field. Going forward, my research will focus on the viral traits which allow transmission to proceed in guinea pigs, a mammalian model system which we have demonstrated to reflect humans well in terms of influenza virus transmissibility.
Jessica Trost, BS
Jessica Trost received her BS in Biology from the University of Wisconsin-Madison in 2007. After graduation, she pursued work in pediatric respiratory virus research and clinical diagnostic development at the Medical College of Wisconsin. Following the 2009 influenza pandemic, and inspired by the importance of preparedness, she applied and was awarded the APHL/CDC Emerging Infectious Disease (EID) fellowship at CDC and joined the Influenza Division. At CDC, her work included detecting and evaluating potentially broadly neutralizing antibodies in influenza, vaccine strain selection, and the first evidence of influenza infection in sea otters. Her current research at Emory University as a student in the Microbiology and Molecular Genetics (MMG) program in Dr. David Steinhauer’s lab focuses on understanding the relationship and balance of the two major surface glycoproteins of influenza, HA and NA. Her aim is to understand the impact of these two proteins in the reassortment and emergence of novel and pandemic influenza viruses from natural avian reservoirs. With the support of the Antimicrobial Resistance and Therapeutic Discovery Training Program, she hopes to evaluate the potential for novel influenza subtypes to emerge in naive human populations, or reassort with current influenza strains in humans, to highlight and improve vaccine and antiviral targets in advance of emerging epidemics and pandemics.
David Steinhauer, PhD
The Steinhauer laboratory is primarily interested in influenza virus entry into host cells and the role of the hemagglutinin glycoprotein (HA) in this process. The work has a strong focus on the structure-function relationships of HA with regard to its receptor binding and membrane fusion properties. The work combines protein structure analysis and molecular virology techniques to address specific questions on how influenza viruses attach to cells, deliver their genomes, assemble at the end of the replication cycle, and evolve to evade host immune responses and the action of antiviral drugs. We are also attempting to exploit our knowledge of high resolution HA structures to design novel vaccines for influenza, and for other pathogens using influenza as a vector.