Abstract

application). The Molecular Virology Core will have three distinct functions to support research on the human hepatocyte cell culture model of HCV replication and liver cell injury. The three functions of the Molecular Virology Core are: 1) to provide HCV RNA from infectious clone sources and viremic sera from infected patient sources for use in infectivity studies; 2) to characterize HCV replication in the human hepatocyte model by quantitative assessment of HCV genome and antigenome production; and 3) track propagation of HCV quasispecies variants in hepatocyte culture by heteroduplex mobility analysis and nucleotide sequencing. These functions are also components of the other sections of the application, and in this regard the Molecular Virology Core will be a service facility. In addition, several key hypotheses on HCV infectivity and viral determinants of hepatocellular injury will be explored.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Allergy and Infectious Diseases (NIAID)
Type
Research Program--Cooperative Agreements (U19)
Project #
1U19AI048214-01
Application #
6356699
Study Section
Special Emphasis Panel (ZAI1-LIG-M (M1))
Project Start
2000-09-01
Project End
2005-08-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2000
Total Cost
$212,228
Indirect Cost

  Institution

Name
University of Washington
Department
Type
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195

  Publications

Bruden, Dana J T; McMahon, Brian J; Townshend-Bulson, Lisa et al. (2017) Risk of end-stage liver disease, hepatocellular carcinoma, and liver-related death by fibrosis stage in the hepatitis C Alaska Cohort. Hepatology 66:37-45
Li, Hui; Hughes, Austin L; Bano, Nazneen et al. (2011) Genetic diversity of near genome-wide hepatitis C virus sequences during chronic infection: evidence for protein structural conservation over time. PLoS One 6:e19562
McMahon, Brian J; Bruden, Dana; Bruce, Michael G et al. (2010) Adverse outcomes in Alaska natives who recovered from or have chronic hepatitis C infection. Gastroenterology 138:922-31.e1
Joyce, Michael A; Walters, Kathie-Anne; Lamb, Sue-Ellen et al. (2009) HCV induces oxidative and ER stress, and sensitizes infected cells to apoptosis in SCID/Alb-uPA mice. PLoS Pathog 5:e1000291
Walters, Kathie-Anne; Syder, Andrew J; Lederer, Sharon L et al. (2009) Genomic analysis reveals a potential role for cell cycle perturbation in HCV-mediated apoptosis of cultured hepatocytes. PLoS Pathog 5:e1000269
Li, Hui; McMahon, Brian J; McArdle, Susan et al. (2008) Hepatitis C virus envelope glycoprotein co-evolutionary dynamics during chronic hepatitis C. Virology 375:580-91
Li, Hui; Thomassen, Lisa V; Majid, Ayaz et al. (2008) Investigation of putative multisubtype hepatitis C virus infections in vivo by heteroduplex mobility analysis of core/envelope subgenomes. J Virol 82:7524-32
Sullivan, Daniel G; Bruden, Dana; Deubner, Heike et al. (2007) Hepatitis C virus dynamics during natural infection are associated with long-term histological outcome of chronic hepatitis C disease. J Infect Dis 196:239-48
Kash, John C; Goodman, Alan G; Korth, Marcus J et al. (2006) Hijacking of the host-cell response and translational control during influenza virus infection. Virus Res 119:111-20
Walters, Kathie-Anne; Smith, Maria W; Pal, Sampa et al. (2006) Identification of a specific gene expression pattern associated with HCV-induced pathogenesis in HCV- and HCV/HIV-infected individuals. Virology 350:453-64

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