14th ICID - Poster Abstracts - International Society for Infectious ...

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When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 84.015 Session: Virology and Viral Infections (Non-HIV) Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation A description of the pathogenesis associated with pirital virus (an arenavirus) infection in the Syrian golden hamster R. Stammen, J. Garver, S. Sarrazine, E. Vela Battelle , Columbus, OH, USA Background: Arenaviruses are rodent-borne agents and some are capable of causing hemorrhagic fever in humans. These viruses cause acute or persistent infection in a diverse range of animals. Research involving arenaviruses that induce hemorrhagic fever is normally performed in a BSL-4 laboratory environment. However, BSL-2/3 arenaviruses that cause hemorrhagic fever in animals may be used as a surrogate model system to screen potential vaccines and/or therapeutics. Pirital virus (PIRV) is a BSL-3 New World arenavirus that induces hemorrhagic fever manifestations in the Syrian golden hamster model. This model can be utilized to screen and test vaccines and therapeutics. Methods: Female Syrian golden implanted with telemetry units measuring temperature and activity were followed for 14 days post-challenge. Clinical signs of disease were monitored. Viral titers in tissues, viremia, clinical chemistry, hematology, and coagulation parameters and analyzed. Results: Intraperitoneal infection of female Syrian golden hamsters with PIRV led to a specific disease progression involving fever, loss of weight, lethargy, petechial rashes, huddled posture, ruffled fur, epistaxis, and orbital hemorrhaging. Animals surviving to the later stages of disease exhibited whole body tremors, loss of balance, shaking, hind limb paralysis, and rectal hemorrhaging. PIRV infection in hamsters results in 100% mortality in 6-8 days after challenge and analyses of tissues resulted in measureable viremia and viral titers in the adrenals, lymph nodes, intestines, kidney, liver, and brain. Changes in clinical chemistry parameters suggest liver and kidney damage while coagulation parameters demonstrate a disruption of coagulation and clotting. Hematology data demonstrate an increase in white blood cell (WBC) and an increase or stabilization of thrombocytic counts. Conclusion: In all, this has led to a description of a hemorrhagic fever model to study arenavirus hemorrhagic fever pathogenesis and can be used as a cost effective, time-efficient BSL-3 surrogate to screen various antiviral therapeutics and/or vaccine strategies.
When citing these abstracts please use the following reference: Author(s) of abstract. Title of abstract [abstract]. Int J Infect Dis 2010;14S1: Abstract number. Please note that the official publication of the International Journal of Infectious Diseases 2010, Volume 14, Supplement 1 is available electronically on http://www.sciencedirect.com Final Abstract Number: 84.016 Session: Virology and Viral Infections (Non-HIV) Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Modification of the type I interferon and proinflammatory cytokine responses by enterovirus 71 Y.-P. Lee 1 , S.-W. Huang 1 , Y.-F. Wang 2 , C.-K. Yu 1 1 National Cheng Kung University, Tainan City, Taiwan, R.O.C., 2 National Health Research Institute, Tainan City, Taiwan, R.O.C. Background: Enterovirus 71 (EV71) is a neutropic virus targeting the brain stem that may result in severe sequelae including paralysis and pulmonary edema (PE). Type I interferons (IFNs) represent an essential innate defense mechanism for controlling EV71 infection. Inflammatory response with induction of toxic inflammatory cytokines has been considered as an essential component of the pathogenesis of EV71, especially the development of neurogenic PE. Methods: In this study, the role of the type I IFN and proinflammatory cytokine responses on the disease development and mechanisms of viral evasion were investigated by using a murine model with mouse-adapted EV71 strain. Results: After EV71 inoculation, the animals developed viremia, limb paralysis, pulmonary dysfunction, and emphysema with a significant increase of interleukin (IL)-6, monocyte chemoattractant protein-1, tumor necrosis factor and IFN-, but not IL-10, IL-12, IL-13, and type I IFNs in serum and brain. We assumed that sufficient amounts of PE-associated cytokines (i.e., IL-6, IL-13, and IFN-) may be required for the development of EV71-induced PE. The results showed that EV71-infected mice with post-treatment of IL-6, IL-13, and IFN- developed PE and severe emphysema accompanying with a more severe pulmonary dysfunction than EV71- infected, cytokine non-treated mice. Furthermore, we observed that mice inoculated with EV71 produced a significant lower amount of serum type I IFNs than those inoculated with poly (I:C), adenovirus type V, or Coxsackie B3 virus (CB3). EV71 pre-infection abolished both poly (I:C) and CB3 induced-type I IFN production, and decreased the percentage of IFN-producing plasmacytoid dendritic cells in blood of CB3-infected mice. In addition, a pre-incubation of EV71 also reduced poly (I:C) induced-type I IFN production of murine monocyte/macrophage cell line, RAW264.7. The inhibitory effect of EV71 on type I IFN production was contributed by 3C protease that was proven using over-expression systems either in RAW264.7 cell or adult mouse. Conclusion: In conclusion, EV71 may block type I IFN synthesis through 3C protease to interfere with host innate defence, and on the other hand, trigger proinflammatory cytokine responses to promote PE development.
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