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.
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.
|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|
|Ireton, Reneé C; Gale Jr, Michael (2014) Pushing to a cure by harnessing innate immunity against hepatitis C virus. Antiviral Res 108:156-64|
|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|
|Brownell, Jessica; Bruckner, Jacob; Wagoner, Jessica et al. (2014) Direct, interferon-independent activation of the CXCL10 promoter by NF-*B and interferon regulatory factor 3 during hepatitis C virus infection. J Virol 88:1582-90|
|Horner, Stacy M; Gale Jr, Michael (2013) Regulation of hepatic innate immunity by hepatitis C virus. Nat Med 19:879-88|
|Ireton, Renee C; Gale Jr, Michael (2013) Systems biology analyses to define host responses to HCV infection and therapy. Curr Top Microbiol Immunol 363:143-67|
|Negash, Amina A; Ramos, Hilario J; Crochet, Nanette et al. (2013) IL-1? production through the NLRP3 inflammasome by hepatic macrophages links hepatitis C virus infection with liver inflammation and disease. PLoS Pathog 9:e1003330|
|Patel, Maulik R; Loo, Yueh-Ming; Horner, Stacy M et al. (2012) Convergent evolution of escape from hepaciviral antagonism in primates. PLoS Biol 10:e1001282|
|Loo, Yueh-Ming; Gale Jr, Michael (2011) Immune signaling by RIG-I-like receptors. Immunity 34:680-92|
Showing the most recent 10 out of 13 publications