Select a year 2001 2002 2003    Select a researcher Ernesto Abel-Santos, Ph.D. Christopher F. Basler, Ph.D. Yasmine Belkaid, Ph.D. Keril J. Blight, Ph.D. Michael D. Burkart, Ph.D. Kirk W. Deitsch, Ph.D. Michael S. Diamond, M.D., Ph.D. Philip Ralph Dormitzer, M.D., Ph.D. David A. Fidock, Ph.D. Michael Gale Jr., Ph.D. Michael S. Glickman, M.D. Kristin M. Hager, Ph.D. Claudia Hase, Ph.D. Kent Hill, Ph.D. B. Joseph Hinnebusch, Ph.D. Marc Lipsitch, D.Phil. John D. McKinney, Ph.D. Eleftherios “Terry” Mylonakis, M.D., Ph.D. Karen M. Ottemann, Ph.D. Lalita Ramakrishnan, M.D., Ph.D. Pejman Rohani, Ph.D. Michael Jeffrey Root,, M.D., Ph.D. David S. Schneider, Ph.D. Anita Sil, M.D., Ph.D Joseph D. Smith, Ph.D. Ali A. Sultan, M.D., Ph.D. Jatin M. Vyas, M.D., Ph.D. Paula Watnick, M.D., Ph.D. Elizabeth Winzeler, Ph.D. Fitnat Yildiz, Ph.D. Select a project Genetic Determinants of Chloroquine Resistance in Plasmod...Analysis of membrane trafficking events in the regulation ...Antibiotic Resistance in Streptococcus pneumoniae: Transmi...Antigen Processing and Presentation in the Specialized Ent...Bacterial and Host Contributions to the Maintenance of the...Biosynthetic Inhibition of Small Molecule Virulence Factor...Characterization of the NS4B Protein in Hepatitis C VirusCoordinate regulation of M. tuberculosis cell envelope com...Dissecting malaria vector-pathogen interactions using a Dr...DNA Replication and var gene expression in Plasmodium falc...Emerging Viruses: Interferon-Antagonists and VirulenceEnvironmental factors that modulate biofilm formation dyna...Functional Analysis of the Plasmodium GenomeGenetic Analysis of TB Persistence: Identification of New ...Genome-wide Binding Analysis of the Plasmodium falciparum ...Helicobacter pylori: Proteins and Processes that Contribut...Identification of the Bioenergetics Sensor Affecting Virul...Latency, Reactivation and Immunity in Chronic Parasitic Di...Mechanism and Biology of Trypanosome cell motility: contri...Mechanisms of Hepatitis C Virus PersistenceMechanisms of Yersinia pestis transmission and pathogenicityMolecular Analysis of Detoxification of Nitric Oxide in Molecular Mechanisms of Plasmodium Sporozoite PathogenicityNovel Regulators of Biofilm Development by Vibrio choleraePeptide Modulators of Bacterial Cell DifferentiationStructure-based Approach to Rotavirus Vaccine Design and C...Targeting Viral Entry Using the 5-Helix Protein Design Str...The Ecology and Evolution of Disease InterferenceThe Immunology and Neurobiology of West Nile Encephalitis ...Use of the Caenorhabditis elegans model of fungal p... Select an institution Albert Einstein College of Medicine of Yeshiva University Children's Hospital, Boston Harvard School of Public Health Massachusetts General Hospital Memorial Sloan Kettering Cancer Center Mount Sinai School of Medicine National Institute of Allergy and Infectious Disease, National Institutes of Health Oregon State University Rockefeller University Scripps Research Institute Seattle Biomedical Research Institute Stanford University School of Medicine Thomas Jefferson University Tufts University School of Medicine University of California - Los Angeles University of California - San Diego University of California - San Francisco University of California - Santa Cruz University of Cincinnati College of Medicine University of Georgia Research Foundation, Inc. University of Notre Dame University of Texas Southwest Medical Center University of Washington School of Medicine Washington University Washington University School of Medicine Weill Medical College of Cornell University

Kirk W. Deitsch, Ph.D. Weill Medical College of Cornell University

Malaria continues to be a disease of extreme importance in the developing world, infecting 300-500 million people yearly and resulting in 1-2 million deaths, primarily of young African children. The vast majority of malaria morbidity and mortality is caused by infection with the mosquito borne protozoan parasite Plasmodium falciparum. This parasite multiplies within the red blood cells of its host, causing disease through anemia resulting from red cell destruction and also through alterations made to the surface of infected red cells. These alterations make infected cells cytoadherent or “sticky”, allowing them to adhere to the walls of blood vessels, leading to obstruction of blood flow and such clinical manifestations as the often fatal syndrome of cerebral malaria. In addition, the parasites also continually change the identity of the proteins placed on the surface of infected cells, a process referred to as antigenic variation, thus avoiding the immune response mounted by the host. This process promotes a long term, persistent infection that is difficult for the infected individual to clear.

The proteins responsible for the cytoadherent properties of infected red cells are encoded by a mulitcopy gene family called var. While each parasite contains approximately 50 var genes within its genome, only a single copy is expressed at any given time. Over the course of an infection, expression switches to alternate copies within the family, resulting in antigenic variation and a persistent infection. The molecular mechanisms by which parasites manage to express only a single var gene at a time and how switches in expression are coordinated have remained a mystery since the discovery of the var gene family in 1995. Recent work has implicated changes in the structure of the chromatin that surrounds individual var genes as being important for controlling the _expression of this gene family. Work is now underway to investigate how DNA replication influences chromatin assembly and var gene expression patterns in hopes of shedding light on this important process and perhaps to identify potential targets for intervention.

Contact Dr. Deitsch.