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: 73.002 Session: Animal Models, Pathogenesis & Host Defenses Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Up regulation of IRF-2 in West Nile Virus infection: Implications for establishment of viremia in the brain leading to encephalitis K. L. Yeo, M. L. Ng National University of Singapore, Singapore, Singapore Background: A proportion of patients afflicted with WNV can develop neuromuscular degenerative diseases and potentially fatal encephalitis. However, host immuno-modulatory factors involved in the establishment of viremia and subsequent infiltration of cytotoxic immune cells is yet well understood. This study thus investigates the role of IRF-2, an attenuator of interferon (IFN) response, on the establishment of viremia and immune cell infiltration during WNV infection. Methods: Real-time PCR, Western blot, and FACS analyses were used to study the regulation of various IRFs and downstream targets during WNV infection of an astrocytic cell line, A172. Regulation of IRF-2 at the cellular level was then studied using immuno-fluorescence microscopy. Subsequently, cell lines over-expressing, or with a knockdown of IRF-2 were infected to study the effect(s) that IRF-2 has on WNV production. Finally NK cell assay was performed to investigate the ability of NK cells to lyse these infected cells. Results: The IRFs 1, 2, 3 and 7 are highly up regulated post-WNV infection. Expectedly, downstream gene targets like IFN-, IL-12 and IL-6 are up regulated transcriptionally and translationally. In addition, concomitant increased mRNA expression of MHC Class I loading genes like TAP1, TAP2 and 2m with that of HLA-E, translated to an increased surface expression of HLA-E. Interestingly, FACS dot plot analysis revealed that expression of IRF-2 was insufficient to suppress HLA-E expression. Immuno-fluorescence microscopy further showed the surprising preferential enhanced expression of IRF-2 in the non-infected cells. Finally, infection of IRF-2 over-expressing cells resulted in increased virus production, while a reduction in virus titer was observed in the IRF-2 knockdown cells. Conclusion: Our results show that IRF-2 is preferentially up regulated in the neighboring noninfected cells, possibly in a homeostatic fashion to regulate pro-inflammatory genes like IFN and cytokines in these cells. On the other hand, the activated activators overwhelm the attenuation effect(s) of IRF-2 in the infected cells. In these infected cells, the inhibitor of NK cell lysis, HLA-E, is expressed. Its expression thus protects the infected cells from the cytotoxic effects of NK cells. Predisposition of neighboring cells to NK cell lysis and / or subsequent infection thus contributes to overall WNV pathogenesis.
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: 73.003 Session: Animal Models, Pathogenesis & Host Defenses Date: Friday, March 12, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Crimean-Congo hemorrhagic fever virus infects human hepatocytes and induces IL-8 secretion R. Rodrigues 1 , G. Paranhos-Baccala 1 , C. Peyrefitte 2 1 Fondation Merieux, Lyons, France, 2 Fondation Merieux/Institut de recherche Biomedicale des Armees-antenne de Grenoble, Lyons, France Background: Crimean-Congo hemorrhagic fever virus (CCHFV) is a very pathogenic tick-borne virus member of the Bunyaviridae family and the Nairovirus genus. The knowledge of CCHFV pathogenesis is improving: recently, new target cells were identified. We and others had demonstrated that CCHFV is able to infect and partially activate monocytes derived dendritic cells and macrophages. During one retrospective study, it was shown that CCHFV was detected in the liver of infected patients. Methods: Attempting to find other target cells to better understand the pathogenesis of CCHFV, we analyzed the host response induced by CCHFV in hepatocytes infected in vitro during a kinetic study. Results: We noticed that while in HuH7 CCHFV infection elicited a cytopathogenic effect, no visible effect was seen in CCHFV infected HepG2. This intriguing feature led us to analyse the viral parameters expecting a differential cellular response. HuH7 and HepG2 both were shown to be permissive to CCHFV and to replicate the virus at a high load as monitored by plaque titration assay, genomic and anti-genomic strand quantification. The high secretion of IL-8 but no other inflammatory cytokines such as TNF-a, IL-1b indicated that CCHFV induced a response in both hepatocytes. Interestingly, no type I IFN was detected during the kinetic study. In spite of these similarities, we observed a pro-apoptotic CCHF effect more significant in Huh7 than in HepG2 cell lines. Conclusion: We found that hepatocytes could be considered as CCHFV target cells that could be involved in the pathogenesis disorders. The high IL-8 production by infected hepatocytes associated to the pro-apoptotic effect likely contribute to the disease progress.
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