Overview of Hepatitis C Virus Genome Structure, Polyprotein Processing, and Protein Properties

Author(s):  
K. E. Reed ◽  
C. M. Rice
2012 ◽  
Vol 8 (3) ◽  
pp. e1002561 ◽  
Author(s):  
Tomomi Ando ◽  
Hiromi Imamura ◽  
Ryosuke Suzuki ◽  
Hideki Aizaki ◽  
Toshiki Watanabe ◽  
...  

1994 ◽  
Vol 106 (6) ◽  
pp. 1603-1610 ◽  
Author(s):  
Kojiro Michitaka ◽  
Marilena Durazzo ◽  
Hans L. Tillmann ◽  
Diana Walker ◽  
Thomas Philipp ◽  
...  

2018 ◽  
Vol 34 (2) ◽  
pp. 197-210 ◽  
Author(s):  
Catherine Sodroski ◽  
Brianna Lowey ◽  
Laura Hertz ◽  
T. Jake Liang ◽  
Qisheng Li

1996 ◽  
Vol 9 (2) ◽  
pp. 89-96 ◽  
Author(s):  
FLOR H. PUJOL ◽  
YURY E. KHUDYAKOV ◽  
MARISOL DEVESA ◽  
GRACIELA LEÓN ◽  
LINDA BLITZ-DORFMAN ◽  
...  

1993 ◽  
Vol 4 (6) ◽  
pp. 1288-1293
Author(s):  
D M Burstein ◽  
R A Rodby

The hepatitis C virus genome has been recently sequenced and cloned, allowing the identification of patients exposed to this virus, which is now felt to be the principal cause of "non-A, non-B" hepatitis. The hepatitis B virus has long been implicated in the pathogenesis of several glomerulopathies including membranoproliferative glomerulonephritis, mixed cryoglobulinemia, and membranous glomerulonephritis. Several authors have recently reported an association between hepatitis C virus infection and glomerular disease. The case of a patient with chronic hepatitis C virus infection who developed the nephrotic syndrome 3 months after liver transplantation is described. Serologic testing was significant for an elevated rheumatoid factor, circulating cryoglobulins, and a mildly depressed C4 level. Hepatitis C virus antibody and viral RNA (by polymerase chain reaction) were present in both the serum and cryoglobulin fraction. A renal biopsy demonstrated membranoproliferative glomerulonephritis. It is believed that persistent infection with the hepatitis C virus is responsible for an immune complex-mediated glomerulonephritis in this patient. Because hepatitis C has now been pathogenetically linked to several glomerulopathies, testing for this virus should be considered in the serologic work-up of the patient with glomerulonephritis.


2015 ◽  
Vol 36 (3) ◽  
pp. 159-167 ◽  
Author(s):  
Mohammod Johirul ISLAM ◽  
Keisuke HIKOSAKA ◽  
Hidenao NORITAKE ◽  
Mohammad Khaja Mafij UDDIN ◽  
Mohammed Badrul AMIN ◽  
...  

Gene ◽  
1997 ◽  
Vol 200 (1-2) ◽  
pp. 157-162 ◽  
Author(s):  
Masashi Urabe ◽  
Yoko Hasumi ◽  
Yoji Ogasawara ◽  
Takashi Matsushita ◽  
Nobuhiko Kamoshita ◽  
...  

2009 ◽  
Vol 83 (10) ◽  
pp. 5137-5147 ◽  
Author(s):  
Hiromichi Hara ◽  
Hideki Aizaki ◽  
Mami Matsuda ◽  
Fumiko Shinkai-Ouchi ◽  
Yasushi Inoue ◽  
...  

ABSTRACT Persistent infection with hepatitis C virus (HCV) is a major cause of chronic liver diseases. The aim of this study was to identify host cell factor(s) participating in the HCV replication complex (RC) and to clarify the regulatory mechanisms of viral genome replication dependent on the host-derived factor(s) identified. By comparative proteome analysis of RC-rich membrane fractions and subsequent gene silencing mediated by RNA interference, we identified several candidates for RC components involved in HCV replication. We found that one of these candidates, creatine kinase B (CKB), a key ATP-generating enzyme that regulates ATP in subcellular compartments of nonmuscle cells, is important for efficient replication of the HCV genome and propagation of infectious virus. CKB interacts with HCV NS4A protein and forms a complex with NS3-4A, which possesses multiple enzyme activities. CKB upregulates both NS3-4A-mediated unwinding of RNA and DNA in vitro and replicase activity in permeabilized HCV replicating cells. Our results support a model in which recruitment of CKB to the HCV RC compartment, which has high and fluctuating energy demands, through its interaction with NS4A is important for efficient replication of the viral genome. The CKB-NS4A association is a potential target for the development of a new type of antiviral therapeutic strategy.


1991 ◽  
Vol 29 (10) ◽  
pp. 2175-2179 ◽  
Author(s):  
G G Schlauder ◽  
G J Leverenz ◽  
C W Amann ◽  
R R Lesniewski ◽  
D A Peterson

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