|
Ciesek, S.; von Hahn, T.; Colpitts, C.; Schang, L.; Friesland, M.; Steinmann, J.; Manns, M.; Ott, M.; Wedemeyer, H.; Meuleman, P.; Pietschmann, T. & Steinmann, E. (in press),
'The green tea polyphenol epigallocatechin-3-gallate (EGCG) inhibits hepatitis C virus (HCV) entry', Hepatology
n/a
, n/a
.
[Kurzfassung]
[BibTeX]
[Endnote]
Steinmann, E.; Ciesek, S.; Friesland, M.; TJ, E. & Pietschmann, T. (in press),
'Prolonged Survival of Hepatitis C Virus in the Anesthetic Propofol', Clin Infect Dis
n/a
, n/a
.
[Kurzfassung]
[BibTeX]
[Endnote]
Bankwitz, D.; Steinmann, E.; Bitzegeio, J.; Ciesek, S.; Friesland, M.; Herrmann, E.; Zeisel, M.; Baumert, T.; Keck, Z.; Foung, S.; Pecheur, E. & T, T. P. (2010),
'Hepatitis C virus hypervariable region 1 modulates receptor interactions, conceals the CD81 binding site, and protects conserved neutralizing epitopes', J Virol
84
(84(11))
, 5751-5763
.
[Kurzfassung]
[BibTeX]
[Endnote]
Bitzegeio, J.; Bankwitz, D.; Hueging, K.; Haid, S.; Brohm, C.; Zeisel, M.; Herrmann, E.; Iken, M.; Ott, M.; Baumert, T. & T, T. P. (2010),
'Adaptation of hepatitis C virus to mouse CD81 permits infection of mouse cells in the absence of human entry factors', PLoS Pathog
6
, e1000978
.
[BibTeX]
[Endnote]
Bitzegeio, J.; Bankwitz, D.; Hueging, K.; Haid, S.; Brohm, C.; Zeisel, M. B.; Herrmann, E.; Iken, M.; Ott, M.; Baumert, T. F. & Pietschmann, T. (2010),
'Adaptation of hepatitis C virus to mouse CD81 permits infection of mouse cells in the absence of human entry factors', PLoS Pathog
6
, e1000978
.
[Kurzfassung]
[BibTeX]
[Endnote]
Hepatitis C virus (HCV) naturally infects only humans and chimpanzees. The determinants responsible for this narrow species tropism are not well defined. Virus cell entry involves human scavenger receptor class B type I (SR-BI), CD81, claudin-1 and occludin. Among these, at least CD81 and occludin are utilized in a highly species-specific fashion, thus contributing to the narrow host range of HCV. We adapted HCV to mouse CD81 and identified three envelope glycoprotein mutations which together enhance infection of cells with mouse or other rodent receptors approximately 100-fold. These mutations enhanced interaction with human CD81 and increased exposure of the binding site for CD81 on the surface of virus particles. These changes were accompanied by augmented susceptibility of adapted HCV to neutralization by E2-specific antibodies indicative of major conformational changes of virus-resident E1/E2-complexes. Neutralization with CD81, SR-BI- and claudin-1-specific antibodies and knock down of occludin expression by siRNAs indicate that the adapted virus remains dependent on these host factors but apparently utilizes CD81, SR-BI and occludin with increased efficiency. Importantly, adapted E1/E2 complexes mediate HCV cell entry into mouse cells in the absence of human entry factors. These results further our knowledge of HCV receptor interactions and indicate that three glycoprotein mutations are sufficient to overcome the species-specific restriction of HCV cell entry into mouse cells. Moreover, these findings should contribute to the development of an immunocompetent small animal model fully permissive to HCV.
Burgel, B.; Friesland, M.; Koch, A.; Manns, M.; Wedemeyer, H.; Weissenborn, K.; Schulz-Schaeffer, W.; Pietschmann, T.; Steinmann, E. & S, S. C. (2010),
'Hepatitis C virus enters human peripheral neuroblastoma cells - evidence for extra-hepatic cells sustaining hepatitis C virus penetration', J Viral Hepat
(18(8))
.
[Kurzfassung]
[BibTeX]
[Endnote]
Bürgel, B.; Friesland, M.; Koch, A.; Manns, M. P.; Wedemeyer, H.; Weissenborn, K.; Schulz-Schaeffer, W. J.; Pietschmann, T.; Steinmann, E. & Ciesek, S. (2010),
'Hepatitis C virus enters human peripheral neuroblastoma cells - evidence for extra-hepatic cells sustaining hepatitis C virus penetration', J Viral Hepat
.
[Kurzfassung]
[BibTeX]
[Endnote]
Summary. Patients with chronic hepatitis C virus (HCV) infection show an increased incidence of nervous system disorders such as chronic fatigue syndrome, depression and cognitive dysfunction. It is unclear whether this is because of HCV replication in the brain and in peripheral neuronal cells or to more indirect effects of HCV infection on the central or peripheral nervous system. The aim of this study was to investigate whether cells originating from these tissues are permissive for HCV cell entry, RNA replication and virus assembly. Among eight cell lines analysed, the human peripheral neuroblastoma cell line SKNMC expressed all HCV entry factors and was efficiently infected with HCV pseudoparticles (HCVpp) independent of the HCV genotype. All remaining cell types including human neuroblastoma and glioblastoma cell lines and microglial cells lacked expression of at least one host factor essential for HCV entry. When transfected with HCV luciferase reporter virus RNA, inoculated with HCV reporter viruses or challenged with high-titre cell culture-derived HCV, none of these cells supported detectable HCV RNA replication. Thus, in conclusion, this comprehensive screening did not reveal evidence directly strengthening the notion that HCV enters and replicates in the central nervous system. However, productive viral entry into the peripheral neuroblastoma cell line SKNMC indicates that HCV may penetrate into certain nonhepatic cell types which may serve as viral reservoirs and could modulate viral pathogenesis.
Ciesek, S.; Steinmann, E.; Iken, M.; Ott, M.; Helfritz, F.; Wappler, I.; Manns, M.; Wedemeyer, H. & T, T. P. (2010),
'Glucocorticosteroids increase cell entry by hepatitis C virus', Gastroenterology
138
(5)
, 1875-1884
.
[Kurzfassung]
[BibTeX]
[Endnote]
Ciesek, S.; Friesland, M.; Steinmann, J.; Becker, B.; Wedemeyer, H.; Manns, M.; Pietschmann, T. & Steinmann, E. (2010),
'How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides', J Infect Dis
201
(12)
, 1859-1866
.
[BibTeX]
[Endnote]
Ciesek, S.; Friesland, M.; Steinmann, J.; Becker, B.; Wedemeyer, H.; Manns, M. P.; Steinmann, J.; Pietschmann, T. & Steinmann, E. (2010),
'How stable is the hepatitis C virus (HCV)? Environmental stability of HCV and its susceptibility to chemical biocides', J Infect Dis
201
(201(12))
, 1859-1866
.
[Kurzfassung]
[BibTeX]
[Endnote]
In the absence of a cell culture system for propagation of the hepatitis C virus (HCV), the antiviral activity of disinfectants against HCV was extrapolated from studies with the bovine viral diarrhea virus. The recent development of an HCV infection system allowed the direct assessment of environmental stability and susceptibility to chemical disinfectants.Studies were performed using cell-culture grown HCV. Infectivity was determined by limiting dilutions. HCV RNA levels were analyzed by quantitative real-time polymerase chain reaction. Genome stability was determined by transfection of recovered RNA into Huh7.5 cells and immunostaining.HCV infectivity in a liquid environment was detectable for up to 5 month at lower temperatures. The risk of HCV infections may not accurately be reflected by determination of HCV RNA levels, because viral infectivity and HCV RNA copy numbers did not directly correlate. Different alcohols and commercially available antiseptics reduced the infectivity of HCV to undetectable levels. However, diluting the hand disinfectants abrogated the virucidal activity.This study assessed the environmental stability and susceptibility to chemical biocides of HCV. The results should be useful in defining rigorous disinfection protocols to prevent nosocomial transmission of HCV.
Hahn, T.; Steinmann, E.; Ciesek, S. & T, T. P. (2010),
'Know your enemy: translating insights about the molecular biology of hepatitis C virus into novel therapeutic approaches', Expert Rev Gastroenterol Hepatol
4
(4(1))
, 63-79
.
[Kurzfassung]
[BibTeX]
[Endnote]
Haid, S.; Windisch, M.; Bartenschlager, R. & Pietschmann, T. (2010),
'Mouse-specific residues of claudin-1 limit hepatitis C virus genotype 2a infection in a human hepatocyte cell line', J Virol
84
(84(2))
, 964-975
.
[Kurzfassung]
[BibTeX]
[Endnote]
Lemon, S.; McKeating, J.; Pietschmann, T.; Frick, D.; Glenn, J.; Tellinghuisen, T.; Symons, J. & Furman, P. (2010),
'Development of novel therapies for hepatitis C', Antiviral Res
86
(86(1))
, 79-92
.
[Kurzfassung]
[BibTeX]
[Endnote]
Montserret, R.; Saint, N.; Vanbelle, C.; Salvay, A.; Simorre, J.; Ebel, C.; Sapay, N.; Renisio, J.; Bockmann, A.; Steinmann, E.; Pietschmann, T.; Dubuisson, J.; Chipot, C. & Penin, F. (2010),
'NMR structure and ion channel activity of the p7 protein from hepatitis C virus', Biol Chem
285
(285(41))
, 31446-31461
.
[Kurzfassung]
[BibTeX]
[Endnote]
Stegmann, K.; Bjorkstrom, N.; Veber, H.; Ciesek, S.; Riese, P.; Wiegand, J.; Hadem, J.; Suneetha, P.; Jaroszewicz, J.; Wang, C.; Schlaphoff, V.; Fytili, P.; Cornberg, M.; Manns, M.; Geffers, R.; Pietschmann, T.; Guzman, C.; Ljunggren, H. & Wedemeyer, H. (2010),
'Interferon-alpha-induced TRAIL on natural killer cells is associated with control of hepatitis C virus infection', Gastroenterology
138
(5)
, 1885-1897
.
[Kurzfassung]
[BibTeX]
[Endnote]
Steinmann, J.; Becker, B.; Bischoff, B.; Paulmann, D.; Friesland, M.; Pietschmann, T. & E, E. S. (2010),
'Virucidal activity of 2 alcohol-based formulations proposed as hand rubs by the World Health Organization', Am J Infect Control
38
(38(1))
, 66-68
.
[Kurzfassung]
[BibTeX]
[Endnote]
Brohm, C.; Steinmann, E.; Friesland, M.; Lorenz, I.; Patel, A.; Penin, F.; Bartenschlager, R. & Pietschmann, T. (2009),
'Characterization of determinants important for hepatitis C virus p7 function in morphogenesis using trans-complementation', J Virol
83
(83(22))
, 11682-93
.
[Kurzfassung]
[BibTeX]
[Endnote]
Ciesek, S.; Steinmann, E.; Wedemeyer, H.; Manns, M.; Neyts, J.; Tautz, N.; Madan, V.; Bartenschlager, R.; von Hahn, T. & Pietschmann, T. (2009),
'Cyclosporine A inhibits hepatitis C virus nonstructural protein 2 through cyclophilin A', Hepatology
50
(5)
, 1638-1645
.
[Kurzfassung]
[BibTeX]
[Endnote]
Haid, S.; Pietschmann, T. & Pecheur, E. (2009),
'Low pH-dependent hepatitis C virus membrane fusion depends on E2 integrity, target lipid composition, and density of virus particles', Pecheur EI Haid S
284
(284(26))
, 17657-17667
.
[Kurzfassung]
[BibTeX]
[Endnote]
Haybaeck, J.; Zeller, N.; Wolf, M.; Weber, A.; Wagner, U.; Kurrer, M.; Bremer, J.; Iezzi, G.; Graf, R.; Clavien, P.; Thimme, R.; Blum, H.; Nedospasov, S.; Zatloukal, K.; Ramzan, M.; Ciesek, S.; Pietschmann, T.; Marche, P.; Karin, M.; Kopf, M.; Browning, J.; Aguzzi, A. & M, M. H. (2009),
'A lymphotoxin-driven pathway to hepatocellular carcinoma', Cancer Cell
16
(16(4))
, 295-308
.
[Kurzfassung]
[BibTeX]
[Endnote]
Pietschmann, T. (2009),
'Full-length infectious HCV chimeras', Methods Mol Biol
510
, 347-359
.
[Kurzfassung]
[BibTeX]
[Endnote]
Pietschmann, T.; Zayas, M.; Meuleman, P.; Long, G.; Appel, N.; Koutsoudakis, G.; Kallis, S.; Leroux-Roels, G.; Lohmann, V. & R, R. B. (2009),
'Production of infectious genotype 1b virus particles in cell culture and impairment by replication enhancing mutations', PLoS Pathog
5
(5(6))
, e1000475
.
[Kurzfassung]
[BibTeX]
[Endnote]
Pietschmann, T. (2009),
'Regulation of hepatitis C virus replication by microRNAs', J Hepatol
50
(50(3))
, 441-444
.
[Kurzfassung]
[BibTeX]
[Endnote]
Pietschmann, T. (2009),
'Virology: Final entry key for hepatitis C', Nature
457
(7231)
, 797-798
.
[Kurzfassung]
[BibTeX]
[Endnote]
Witteveldt, J.; Evans, M.; Bitzegeio, J.; Koutsoudakis, G.; Owsianka, A.; Angus, A.; Keck, Z.; Foung, S.; Pietschmann, T.; Rice, C. & Patel, A. (2009),
'CD81 is dispensable for hepatitis C virus cell-to-cell transmission in hepatoma cells', Virol J Gen
90
(90(Pt 1))
, 48-58
.
[Kurzfassung]
[BibTeX]
[Endnote]
|
