An efficient administrative structure is essentia! to the design and implementation of this U19 Program. The Administrative Core is designed to facilitate communication, planning, data sharing, and scientific and fiscal oversight of the component research projects of the Program. Through Core A, the Core Director will oversee all the goals of this research Program. The Core Director will serve as the primary contact between project investigators, and will serve as the liaison between this research group and the NIH program staff. The Core will facilitate the Program's compliance with NIH and institutional policies, grants management, and will fund yearly travel of the Program investigators to Bethesda and Seattle for the annual extemai and internal review of the Program, respectively. The Core will include a Project Manager who will coordinate, schedule, and implement minimum monthly internal meetings and teleconferencing among the Program sites, and will prepare progress reports, internal compliance filings and edit manuscripts to support the Program. The Core will oversee data sharing, data archiving, and overall record keeping of the Program.

Public Health Relevance

The Administrative Core will play an important role to facilitate the scientific and fiscal management ofthe U19 research Program. The Program is focused on defining the virus-host interactions that control innate immunity against Hepatitis C virus (HCV). This work is important because HCV infects nearly 200 million people across the globe and is thus a major public health threat. The Administrative Core will serve the Program to mediate efficient communication and scientific discussion between the Project investigators and the NIH staff to support our goal of improving the outcome of HCV infection and antiviral therapy.

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
5U19AI088778-04
Application #
8447524
Study Section
Special Emphasis Panel (ZAI1-BP-M)
Project Start
Project End
Budget Start
2013-04-01
Budget End
2014-03-31
Support Year
4
Fiscal Year
2013
Total Cost
$43,356
Indirect Cost
$7,068
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
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Kell, Alison M; Gale Jr, Michael (2015) RIG-I in RNA virus recognition. Virology 479-480:110-21
Horner, Stacy M; Wilkins, Courtney; Badil, Samantha et al. (2015) Proteomic analysis of mitochondrial-associated ER membranes (MAM) during RNA virus infection reveals dynamic changes in protein and organelle trafficking. PLoS One 10:e0117963
Chakrabarti, Arindam; Banerjee, Shuvojit; Franchi, Luigi et al. (2015) RNase L activates the NLRP3 inflammasome during viral infections. Cell Host Microbe 17:466-77
Kell, Alison; Stoddard, Mark; Li, Hui et al. (2015) Pathogen-Associated Molecular Pattern Recognition of Hepatitis C Virus Transmitted/Founder Variants by RIG-I Is Dependent on U-Core Length. J Virol 89:11056-68
Errett, John S; Gale, Michael (2015) Emerging complexity and new roles for the RIG-I-like receptors in innate antiviral immunity. Virol Sin 30:163-73
Negash, Amina A; Gale Jr, Michael (2015) Hepatitis regulation by the inflammasome signaling pathway. Immunol Rev 265:143-55
Wieland, S F; Takahashi, K; Boyd, B et al. (2014) Human plasmacytoid dendritic cells sense lymphocytic choriomeningitis virus-infected cells in vitro. J Virol 88:752-7
Wieland, Stefan; Makowska, Zuzanna; Campana, Benedetta et al. (2014) Simultaneous detection of hepatitis C virus and interferon stimulated gene expression in infected human liver. Hepatology 59:2121-30
McFarland, Adelle P; Horner, Stacy M; Jarret, Abigail et al. (2014) The favorable IFNL3 genotype escapes mRNA decay mediated by AU-rich elements and hepatitis C virus-induced microRNAs. Nat Immunol 15:72-9

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