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: 24.011 Session: Arboviruses Date: Wednesday, March 10, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation Association of tumor necrosis factor-alpha gene promoter regions polymorphism in Japanese encephalitis patients S. K. Pujhari 1 , R. K. Ratho 2 , S. Prabhakar 1 , B. Mishra 1 , M. sharma 1 , M. Modi 1 1 Postgraduate Institute of Medical Education and Research, 160012, UT, India, 2 Postgraduate Institute of medical Education and Research, 160012, India Background: More than three billion populations are living under the threat of Japanese encephalitis in the south East Asian countries including India. The pathogenesis of this disease is not clearly understood, and is possibly attributed to the genomic variation in virus as well the host genetic make up. The present study focused to determine the role of -238G/A, -857C/T and - 863C/A polymorphism of tumor necrosis factor-alpha (TNF-a), gene promoter polymorphism in Japanese encephalitis patients as a part of host role in disease severity and pathogenesis. Methods: Twenty encephalitis cases (PCR/IgM positive) 16 JE IgM positive fever cases with out encephalitis were considered as subject group I and II respectively, and from A 46 healthy individuals were taken as controls. The genomic DNA was extracted from whole blood/clotted blood. TNF-a promoter polymorphism was performed by PCR restriction fragment length polymorphism. The statistical analysis was performed by X2 using GraphPad software. Results: The genotype frequencies of C/C at -863 are 90 % and 93.75% in subject group I and II respectively and 47.83% in controls. The distribution AA in subject group I and II are 10% and 6.25% respectively and 32.61% in control, in fever and in encephalitis patients. Where as distribution of C/A was found only in controls (19.56%). Significantly higher frequency of distribution was observed in JE encephalitis (Subject group I) and fever cases (Subject group II) as compared to that of healthy controls (X2 10.522, p=0.005, X2 10.77, p= =< 0.005). The frequency of C/C at-857 are in the range of 65.22 to 75%, of C/T are 15% to 32.6%, where as the frequency distributions of G/G at –238 position are in the range of 87.5% to 100% and of G/A 6.25% to 12.5% There was no difference observed in the subjects and control groups. Conclusion: With the available TNF-a promoter variations data analysis reveals that position - 863promoter likely to play a substantial role in severity of Japanese encephalitis viral infection.
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: 24.012 Session: Arboviruses Date: Wednesday, March 10, 2010 Time: 12:30-13:30 Room: Poster & Exhibition Area/Ground Level Type: Poster Presentation A novel antagonistic relationship between human Sec3 exocyst and flavivirus capsid protein B. Raghavan, K. L. Yeo, M. L. Ng National University of Singapore, Singapore, Singapore Background: The Flaviviridae family comprises several medically important pathogens such as West Nile virus (WNV) and Dengue virus (DENV). Flavivirus capsid (C) protein is a key structural component of virus particles. However, the role of C protein in the pathogenesis of arthropodborne flaviviruses is poorly understood. Examination of whether flavivirus C protein can associate with cellular proteins and contribute to viral pathogenesis would define the platform towards the development of new anti-virals against flavivirus infection. Methods: Yeast-two-hybrid screening of brain library was employed to identify the host interacting partners of WNV/DENV C protein. Co-immunoprecipitation and mutagenesis studies were used to delineate the interacting domains of host and C proteins. We used a combination of lentivirus-mediated gene knock-down/over-expression analyses, real-time RT-PCR, coimmunoprecipitation, Western blotting, densitometry, pull-down, proteasome activity and competition assays to unveil the biological significance of identified host-C protein association. Results: This study identified human Sec3 exocyst protein (hSec3p) as a novel interacting partner of WNV/ DENV C protein. Mutagenesis studies showed that SH2 domain-binding motif of hSec3p binds to the first 15 amino acids of C protein. We reported that hSec3p can modulate virus production by affecting viral RNA transcription and translation through the sequestration of elongation factor 1 alpha (EF1). We also demonstrated that flavivirus C protein degrades hSec3p through proteasome-mediated pathway. Conclusion: This study highlighted for the first time that hSec3p functions as a new transcriptional and translational repressor of flavivirus replication. Our study also demonstrated that flavivirus C protein plays an important role in nullifying the antiviral checkpoints imposed by hSec3p and allowing the virus to establish a microenvironment that facilitates successful replication and infection. Understanding the molecular mechanism of flavivirus C protein and hSec3p interaction, besides revealing the new cellular functions of hSec3p, could possibly pave the way towards the development of potential hSec3p-derived antiviral agent against flaviviruses.
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