Dr. Deb Brown is an Assistant Professor in the School of Biological Sciences and a member of the Nebraska Center for Virology. Dr. Brown received her PhD at the University of Rochester Medical Center in Rochester, NY and studied under Dr. Suzy Swain as a post-doctoral fellow at the Trudeau Institute. In 2008, she accepted a faculty position at UNL and currently teaches the undergraduate/graduate Immunology course. Dr. Brown’s research has established that CD4 T cells acquire perforin-mediated cytotoxicity (CD4 CTL) in vivo as part of a multifunctional activation program that contributes to protection against lethal influenza infection. The main focus of Dr. Brown’s research is to understand how CD4 T cells are activated, differentiate into effectors and provide protection against viral infections, with the ultimate goal of designing vaccines that provide broad, universal protection against emerging pathogens. Dr. Brown’s research group has demonstrated that the cytokine IL-2 is necessary to induce CTL activity in CD4 cells, but high inflammatory conditions can overcome the requirement for this cytokine. Currently, the lab aims to understand how vaccination shapes the T cell response and promotes survival against lethal influenza infection. Ongoing work is directed at identifying the inflammatory mediators important for generating CD4 CTL in the lung and determining whether CD4 CTL are required for protection in the vaccine model. Dr. Brown is a member of the American Association of Immunologists (AAI) and American Society for Microbiology (ASM). She has been awarded junior faculty travel grants in 2010, 2011 and 2013 for presentations at the AAI national meetings.
W. Ian Lipkin is the John Snow Professor of Epidemiology, Professor of Neurology & Pathology, and Director of the Center for Infection and Immunity (CII) at Columbia University. A graduate of Sarah Lawrence College, he obtained his MD at Rush Medical College, Medicine Residency at the University of Washington, Neurology Residency at the University of California San Francisco, and Fellowship in Microbiology and Neuroscience at The Scripps Research Institute. His contributions include the first use of purely molecular methods to identify an infectious agent; implication of West Nile virus as the cause of the encephalitis in North America in 1999; invention of MassTag PCR and the first panmicrobial microarray; first use of deep sequencing in pathogen discovery; and the discovery and molecular characterization of more than 500 viruses. His honors include the following: Pew Scholar in the Biomedical Sciences, Japanese Human Science Fdn Visiting Prof, Columbia University Visiting Bruenn Prof, Am Soc of Microbiol Fdn Lecturer, Ellison Medical Fdn Senior Scholar in Global Infectious Disease, Fellow of the NY Academy of Sciences, Distinguished Lecturer of the Nat’l Center for Infectious Diseases, Fellow of the Am Soc for Microbiol, John Courage Prof Nat’l University of Singapore, Kinyoun Lecturer NIH, Fellow of the Wildlife Conservation Soc, Fellow of the Am Assoc for the Advancement of Science, Member of the Assoc of Am Physicians and Member of the NIH Advisory Committee to the Director.
My undergraduate work was done at the College of Agriculture of Cornell University. I received my doctorate from Rockefeller University for studies on genetic transformation in Streptococcus pneumonia. Since that time I have been associated with the Public Health Research Institute which is now part of Rutgers university. I only left PHRI for one year that I spent as a visiting investigator at the Pasteur Institute in Paris.
My initial scientific interest was in bacteriophage studies. However I spent a number of years studying microbial cell division and membrane biology. In 1973 I read with great interest a series of papers from the University of Nebraska describing the isolation of a bacteriophage called phi6 that had a lipid containing membrane and a genome of three double-stranded RNA segments. From that time on, I have pursued the study of the biology of phi6 and other members of its family, the Cystoviridae. In particular, my laboratory has been interested in the mechanisms involved in the precise packaging of segmented viral genomes and the temporal control of gene expression. In both cases, the mechanisms have involved unique and interesting structural considerations. Our major contribution has been the elucidation of the mechanism of precise packaging of a segmented viral genome.
Dr. Robert F. Siliciano is a member of the Howard Hughes Medical Institute and a Professor of Medicine and Molecular Biology and Genetics at the Johns Hopkins University School of Medicine. In 1995, his laboratory provided the first demonstration that latently infected memory CD4+ T cells were present in patients with HIV-1 infection. He went on to characterize this latent reservoir and to show that latently infected cells persist even in patient on prolonged highly active antiretroviral therapy (HAART). These studies indicated that eradication of HIV-1 infection with HAART alone would never be possible, a finding which led to a fundamental change in the treatment strategy for HIV-1 infection. This latent reservoir is now widely recognized as the major barrier to curing HIV-1 infection and is the subject of an intense international research effort. Dr. Siliciano’s laboratory has gone on to characterize the different forms of HIV-1 that persist in patients on HAART and to explore potential strategies for eradicating the virus from this and other reservoirs. In addition, Dr. Siliciano’s recent work has provided a theoretical foundation for the success of antiretroviral therapy in controlling HIV-1 replication.
Dr. Siliciano did his undergraduate work at Princeton University and then received his MD and PhD degrees from Johns Hopkins. After a postdoctoral fellowship at Harvard Medical School, he joined the faculty at Johns Hopkins. He is the recipient of a Distinguished Clinical Scientist Award from the Doris Duke Charitable Foundation and two NIH Merit Awards. In 2002, he became an Investigator in the Howard Hughes Medical Institute. He is a past Chairman of the NIH AIDS and Related Research Study Section. He currently directs the MD-PhD Program at Johns Hopkins. In 2008, he received a major award in AIDS research, the Bernard N. Fields Memorial Lecture at the Conference for Retroviruses and Opportunistic Infections.
African swine fever (ASF) is a highly lethal hemorrhagic disease of domestic swine with mortality rates approaching 100%. In nature the causative agent, African swine fever virus (ASFV), persists by cycling between Ornithodoros ticks and wild warthog and bushpig populations in sub-Saharan Africa. ASF, is arguably the most significant disease threat for the swine industry world wide because of this large natural reservoir of virus in Africa, the potential for establishment of endemic infection upon introduction into new regions, the rapid and efficient transmission of disease among pigs and the lack of an ASF vaccine. Recent devastating ASF disease outbreaks in the Caucasus and Russia (2007-to date) highlight this threat.
ASF vaccine development is significantly hindered by large gaps in knowledge of the virus, viral protective antigens and the complexity of virus-host interactions underlying infection and immunity. ASFV, currently the sole member of the Asfarviridae, is a unique and genetically complex DNA virus (~190 Kbp) and, it is the only known DNA arbovirus. Research findings involving characterization of novel ASF viral virulence/host range genes and identification of putative protective viral antigens will be described and discussed in the context of the opportunities they provide for ASF vaccine development and improved disease control