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Host-Pathogen Seminar Series 2010-2011

October 4, 2010

Vern Carruthers, PhD, Associate Professor, Department of Microbiology and Immunology, University of Michigan Medical School

"Pathogenesis of parasitic infections: Mechanisms of cell invasion and survival during infection"

The Carruthers lab seeks to understand invasion and survival strategies employed by microbial pathogens during infection. We use the protozoan Toxoplasma gondii as a model pathogen because of its genetic and biochemical tractability, well defined cellular structure, and the availability of excellent rodent models of disease. Toxoplasma replicates in a remarkable variety of cells and organs, causing encephalitis, pneumonia, myocarditis, ocular disease, and congenital birth defects during acute infection. While disease is seen only in a small fraction of the ~2 billion people infected worldwide, the diagnosis and treatment of toxoplasmosis are suboptimal and the disease remains a significant public health problem. In people with healthy immune status, the parasite typically remains in a chronic, encysted state, but the infection can erupt when immune function is compromised such as individuals with HIV/AIDS, organ transplant recipients, or cancer patients undergoing chemotherapy.



November  15, 2010

Laurie Comstock, PhD, Associate Professor of Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School

“Mechanisms of commensalism among the intestinal Bacteroidales”

The long term goals of the laboratory are to elucidate mechanisms used by members of the intestinal microbiota to establish and maintain symbiotic relationships in the mammalian intestine. We study the Bacteroides species, which are the most abundant Gram-negative bacteria of this ecosystem, in some people accounting for 20% of the total intestinal bacteria.


December  13, 2010

Robert Siliciano, MD, PhD, Professor, Departments of Medicine and Molecular Biology and Genetics, Howard Hughes Medical Institute, Johns Hopkins

"Drug therapy for HIV infection"

Co-sponsored by the OSU Department of Pathology and the Davis Heart and Lung Research Institute

For the staggering number of people infected with HIV-1 (33 million), the best current hope for avoiding the fatal consequences of the infection lies in treatment with highly active antiretroviral therapy (HAART), which consists of combinations of 3 drugs that inhibit specific steps in the virus life cycle.  The benefits of HAART in reducing the morbidity and mortality are clearly documented, but major questions remain about how best to use this therapy and how to make it available to all who need it.  Our lab has shown that in the vast majority of patients, current HAART regimens cannot cure the infection as a result of the existence of a very stable reservoir of latent virus in resting memory CD4+ T cells.  Because HAART is not curative, the treatment of HIV-1 infection is a lifelong challenge.
Unfortunately, problems of drug toxicity and the rapid development of drug resistance make this a formidable problem.  Our current research efforts are directed at understanding the basic molecular mechanisms of HIV-1 latency and drug resistance.  We are searching for drugs that can target the latent form of HIV.  In addition, we are focusing on basic pharmacodynamic principles that explain how antiretroviral drugs work.  We have recently uncovered a previously unrecognized form of intermolecular cooperatively that explains why certain classes of antiretroviral drugs can completely inhibit viral replication and are trying to use this discovery to develop improved therapies for HIV infection.


February  21, 2011

Andrew Camilli, PhD, Professor, Sackler School of Graduate Biomedical Sciences, Tufts University

"Regulation and Mechanisms of Bacterial Virulence"

Co-sponsored by the Nationwide Childrens Research Institute, Center for Microbial Pathogenesis

We use genetic and molecular biological approaches to study the pathogenicity of Vibrio cholerae and Streptococcus pneumoniae. Bacterial gene products expressed during infection are being identified and then characterized with respect to their temporal and spatial patterns of regulation within the host and their roles in pathogenicity. The information obtained will positively impact vaccine and antimicrobial drug development, since we will know which bacterial products are produced during infection, when they are expressed, and in response to which host micro-environments.


April 25, 2011

Larry S. Schlesinger, MD, Samuel Saslaw Professor of Medicine; Director, Division of Infectious Diseases and the Center for Microbial Interface Biology; Director, Medical Scientist Program, The Ohio State University

"MicroRNAs and tuberculosis"

Co-sponsored by Public Health Preparedness for Infectious Diseases (PHPID)

The Schlesinger laboratory focuses on human mononuclear phagocyte interactions with the respiratory pathogen Mycobacterium tuberculosis and related mycobacteria, and more recently Francisella tularensis. Current work is focused on the production and role of mycobacterial cell wall carbohydrates produced in vitro and in vivo (including glycomics and lipidomics) in regulating host inflammatory responses through pattern recognition and phagocytic receptors, pulmonary models of the innate immune response to pathogens (role of surfactant), and the identification of host susceptibility factors for tuberculosis using expression genomics.