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Hepatitis C virus (HCV) circulates as a population of different but closely related genomes: quasispecies nature of HCV genome distribution
, 1992
"... Hepatitis C virus (HCV) circulates as a population of different but closely related genomes: quasispecies nature of HCV genome distribution. ..."
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Cited by 146 (10 self)
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Hepatitis C virus (HCV) circulates as a population of different but closely related genomes: quasispecies nature of HCV genome distribution.
Expression of hepatitis C virus proteins induces distinct membrane alterations including a candidate viral replication complex
- J
, 2002
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Cited by 144 (10 self)
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Structure and organization of the hepatitis C virus genome isolated from human carriers
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Viral discovery and sequence recovery using DNA microarrays
- PLoS Biol
, 2003
"... Because of the constant threat posed by emerging infectious diseases and the limitations of existing approaches used to identify new pathogens, there is a great demand for new technological methods for viral discovery. We describe herein a DNA microarray-based platform for novel virus identification ..."
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Cited by 82 (17 self)
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Because of the constant threat posed by emerging infectious diseases and the limitations of existing approaches used to identify new pathogens, there is a great demand for new technological methods for viral discovery. We describe herein a DNA microarray-based platform for novel virus identification and characterization. Central to this approach was a DNA microarray designed to detect a wide range of known viruses as well as novel members of existing viral families; this microarray contained the most highly conserved 70mer sequences from every fully sequenced reference viral genome in GenBank. During an outbreak of severe acute respiratory syndrome (SARS) in March 2003, hybridization to this microarray revealed the presence of a previously uncharacterized coronavirus in a viral isolate cultivated from a SARS patient. To further characterize this new virus, approximately 1 kb of the unknown virus genome was cloned by physically recovering viral sequences hybridized to individual array elements. Sequencing of these fragments confirmed that the virus was indeed a new member of the coronavirus family. This combination of array hybridization followed by direct viral sequence recovery should prove to be a general strategy for the rapid identification and characterization of novel viruses and emerging infectious disease.
Persistent and transient replication of full-length hepatitis C virus genomes in cell culture
- J
, 2002
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Hepatitis C virus glycoprotein folding: disulfide bond formation and association with calnexin. J Virol. 1996;70:778-786. 2300 HAMAIA et al BLOOD, 15 OCTOBER 2001 z VOLUME 98, NUMBER 8 For personal use only.on September 11, 2016. by guest www.bloodjournal
- Hematology, 2021 L St, NW, Suite 900, Washington DC 20036. Blood (print ISSN 0006-4971, online ISSN 1528-0020), is
"... The hepatitis C virus (HCV) glycoproteins (E1 and E2) are released from the polyprotein by signal pepti-dase-mediated cleavage and interact to form a heterodimer. Since properly folded subunits are usually re-quired for specific recognition and stable oligomer formation, the rate of stable E1E2 comp ..."
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Cited by 65 (19 self)
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The hepatitis C virus (HCV) glycoproteins (E1 and E2) are released from the polyprotein by signal pepti-dase-mediated cleavage and interact to form a heterodimer. Since properly folded subunits are usually re-quired for specific recognition and stable oligomer formation, the rate of stable E1E2 complex formation, which is low, may be limited by the rate of HCV E1 and/or E2 folding. In this study, the folding of the HCV E1 and E2 glycoproteins was monitored by observing the kinetics of intramolecular disulfide bond formation. The association/dissociation of E1 and E2 with calnexin was also examined, since this molecular chaperone appears to play a major role in quality control via retention of incompletely folded or misfolded proteins in the endoplasmic reticulum. Our results indicate that the disulfide-dependent folding of E2 occurs rapidly and appears to be complete upon cleavage of the precursor E2-NS2. In contrast, folding of E1 is slow (>1 h), suggesting that this step may be rate limiting for E1E2 oligomerization. Both HCV glycoproteins associated rapidly with calnexin, but dissociation was slow, consistent with the slow folding and assembly of E1E2 glyco-protein complexes. These results suggest a role for prolonged association with calnexin in the folding and assembly of HCV glycoprotein heterodimer complexes. Hepatitis C virus (HCV), the major causative agent of non-A, non-B hepatitis (10, 40), is an enveloped virus contain-
De novo initiation of RNA synthesis by the RNAdependent RNA polymerase (NS5B) of hepatitis C virus
- J
, 2000
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Involvement of endoplasmic reticulum chaperones in folding of hepatitis C virus glycoproteins
- J
, 1998
"... These include: This article cites 59 articles, 30 of which can be accessed free at: ..."
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Cited by 52 (10 self)
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These include: This article cites 59 articles, 30 of which can be accessed free at:
De novo initiation of RNA synthesis by hepatitis C virus nonstructural protein 5B polymerase
- Downloaded from http://jvi.asm.org/ on February 23, 2013 by PENN STATE UNIV
, 2000
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Humoral immune response to hypervariable region 1 of the putative envelope glycoprotein (gp70) of hepatitis C virus
- Journal of Virology
, 1993
"... We recently found that alterations of amino acids in hypervariable region 1 (HVR1) of the putative envelope glycoprotein (gp7O) of hepatitis C virus (HCV) occurred sequentially in the chronic phase of hepatitis at intervals of several months. This finding suggests that mutations in HVR1 are involved ..."
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Cited by 47 (6 self)
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We recently found that alterations of amino acids in hypervariable region 1 (HVR1) of the putative envelope glycoprotein (gp7O) of hepatitis C virus (HCV) occurred sequentially in the chronic phase of hepatitis at intervals of several months. This finding suggests that mutations in HVR1 are involved in the mechanism of persistent chronic HCV infection involving escape from the immunosurveillance system. To explore this possibility, we examined the humoral immune response to HVR1 with our assay system, in which immuno-precipitation was carried out with sera from patients by using an HVR1 (27-amino-acid) dihydrofolate reductase fusion protein synthesized by in vitro transcription and translation. Results showed that HVR1 contains a sequence-specific immunological epitope that induces the production of antibodies restricted to the specific viral isolate. Furthermore, analysis of the kinetics of the appearance of antibodies in two patients with chronic hepatitis, with whom successive alterations of amino acids of HVR1 have been observed, showed that the titers of anti-HVR1 antibodies usually reached maximal levels several months after the isolation of HCV having the specific sequence of HVR1. This observation suggests that anti-HVR1 antibodies are involved in the genetic drift of HVR1 (minor antigenic variation) by immunoselection. However, the coexistence of HVR1 as an antigen and its specific antibody was sometimes observed. The possibility that HVR1 acts as a neutralizing epitope is discussed.
