A proposed system for the nomenclature of hepatitis C viral genotypes

Simmonds, Peter; Alberti, Alberto; Alter, Harvey J.; Bonino, Ferruccio; Bradley, Daniel W.; Bréchot, Christian; Brouwer, Johannes T.; Chan, Shiu-Wan; Chayama, Kazuaki; Chen, Ding‐Shinn; Choo, Qui‐Lim; Colombo, Massimo; Cuypers, H. T. M.; Date, Taro; Dusheiko, G.; Esteban, Juan Ignacio; Fay, Oscar; Hadziyannis, Stephanos J.; Han, Jang H.; Hatzakis, Angelos; Holmes, Eddie; Hotta, Hak; Houghton, Michael; Irvine, Bruce; Kohara, Michinori; Kolberg, Janice A.; Kuo, George; Lau, Johnson Y.N.; Lelie, P. N.; Maertens, Geert; McOmish, F.; Miyamura, Tatsuo; Mizokami, Masashi; Nomoto, Akio; Prince, Alfred M.; Reesink, H. W.; Rice, Charlie; Roggendorf, Michael; Schalm, Solko W.; Shikata, Toshio; Shimotohno, Kunitada; Stuyver, Lieven; Trépo, Christian; Weiner, Amy J.; Yap, Peng Lee; Urdea, Mickey S.

doi:10.1002/hep.1840190538

Cited by 903 publications

(240 citation statements)

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“…Extensive sequence analysis of coding regions of the HCV genome provides evidence for the existence of at least six major genotypes of HCV, some of which can be further divided into subtypes (Simmonds et al, 1993a;Bukh et al, 1993). These virus types and subtypes differ in their geographical distribution, antigenicity, level of viraemia, the severity of disease produced and in the responsiveness of disease indicators to interferon treatment, with type 1 producing the most severe and intractable infections (reviewed by Dusheiko & Simmonds, 1994). This evidence for clinically relevant differences between virus genotypes has made it important to develop simple and reliable procedures that can identify the genotype of virus in an infected individual, The definitive method for deducing virus genotype is nucleotide sequence analysis of the entire virus genome, although it is more practical to infer virus genotype from the sequence of subgenomic regions using percentage sequence identity or phylogenetic analysis (Simmonds et al, 1994a).…”

Section: Introductionmentioning

confidence: 99%

Variation of the hepatitis C virus 5' non-coding region: implications for secondary structure, virus detection and typing

Smith

Mellor²,

Jarvis³

et al. 1995

Journal of General Virology

219

159

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Variation in the 5' non-coding region (5'NCR) of hepatitis C virus (HCV) was investigated in detail by comparing 314 5'NCR sequences of viruses ofgenotypes 1 to 6. Evidence was obtained for the existence of associations between particular 5'NCR sequence motifs and virus types and subtypes. No recombination was observed between the 5'NCR and coding regions of different genotypes, implying that the sequence of subgenomic regions such as the 5'NCR can be used to deduce virus genotype. The distribution of polymorphic sites within the 5'NCR is used to propose improved oligonucleotide primers for virus detection and quantification that would be equally efficient in detecting RNA of different virus genotypes. The accuracy of two different genotyping methods (RFLP and the line probe assay) based on analysis of sequence polymorphisms in the 5'NCR is predicted from the sequences surveyed to be 97 % and 83 % respectively for types 1 to 6, with higher accuracies for distinguishing between subtypes la/lb, 2a/2b or 3a/3b. Several sites of genotype-specific polymorphism were covariant and maintained the base pairings required for a secondary structure model of the 5"NCR. Other sites of variation suggest minor modifications to this model and have implications for the probable functions of the 5"NCR

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Section: Introductionmentioning

confidence: 99%

Variation of the hepatitis C virus 5' non-coding region: implications for secondary structure, virus detection and typing

Smith

Mellor²,

Jarvis³

et al. 1995

Journal of General Virology

219

159

View full text Add to dashboard Cite

show abstract

“…Sequences were aligned using the CLUSTAL V program. 44 Patient genotype was determined by the criteria of HCV RNA was detected by the addition of 100 mL of avidin horseradish peroxidase conjugate followed by 100 mL of sub-Simmonds et al 45 Briefly, the consensus sequence for each patient was aligned with the published 222-bp NS5 region strate and stopping reagent with the appropriate washing steps included. The optical density of each well was deter-HCV genotype sequences.…”

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confidence: 99%

Intrahepatic hepatitis C RNA levels do not correlate with degree of liver injury in patients with chronic hepatitis C

et al. 1996

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jury. Intrahepatic viral load appears to be significantly The balance between a direct cytopathic effect by hepincreased in patients with genotype 1b. IFN-a treatment atitis C virus (HCV) and immune-mediated injury redoes significantly lower intrahepatic HCV load. (HEPAmains unclear. This report aims to test the following TOLOGY 1996;23:676-687.) hypotheses: (1) that intrahepatic HCV load would correlate with the degree of liver injury; (2) that interferon alfa (IFN-a) would decrease intrahepatic HCV-RNA levPersistent hepatitis C infection results in varying deels. Liver tissues (n Å 56) were obtained from 47 patients grees of chronic liver injury. [1][2][3][4][5][6] Healthy carriers of the with chronic HCV (9 before and after IFN-a therapy). hepatitis C virus (HCV) have been described but seem Total RNA was isolated and quantitated for specific HCV uncommon. 7 The pathogenesis of HCV-induced hepatic RNA by dot-blot polymerase chain reaction (DB-PCR) injury remains unclear and could be attributable to either using a standard curve created from synthetic HCV RNA direct cytopathic damage by HCV 8-10 or immune-mediof known titer to calculate actual RNA levels. A multivar-ated hepatic injury induced by HCV. 1,[11][12][13][14][15] It is possible iate analysis was undertaken to determine the relationthat both may act simultaneously. 16,17ship of intrahepatic HCV-RNA levels with risk factors,One way to identify whether liver damage is attributlength of HCV exposure, and histological injury scores.The confounding effect of HCV genotype was examined able to direct cytopathic damage is to examine whether by direct sequencing of the NS5b region. Liver HCV RNA the degree of viral load correlates with the degree of ranged from 10 2 to 3.1 1 10 7 molecules per microgram liver injury. Most studies addressing this question have total liver RNA. The multiple regression analysis showed measured the amount of HCV in serum. 9,10,12,16,[18][19][20][21] Ideno effect of length of HCV exposure, risk factors, degree ally, HCV-RNA viral load should be estimated directly of bile duct damage, steatosis, or total Scheuer or Kno-from liver tissue itself, because serum levels of virus dell score on RNA levels. No significant confounding ef-may be contributed to and influenced by extrahepatic fect of HCV genotype on the degree of liver injury was sources. Also, the presence of serum immune complexes observed. However, genotype 1b had a significantly may introduce further variables. Doubt has also been higher mean intrahepatic HCV-RNA load compared raised as to the validity of HCV-RNA quantitation in with the other genotypes detected. In the 9 patients who received IFN-a, treatment, 7 had no detectable HCV serum compared with plasma. after treatment. This was associated with a significantAs well as the sample type, the method of HCV quandecrease in intrahepatic HCV-RNA levels (7.57 { 2.53 titation itself is important. A number of techniques 1 10 5 to 1.82 { 1.80 1 10 3 molecules per microgram total have been reported for quantitation of HCV by...

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“…-I Genotyping according to the nomenclature in Simmonds et al (1994). :1: Letter in bold indicates amino acid residue change in relation to that of the reference sequence.…”

Section: Methodsmentioning

confidence: 99%

Human recombinant antibodies specific for hepatitis C virus core and envelope E2 peptides from an immune phage display library

Chan

Bye

Jackson

et al. 1996

Journal of General Virology

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Hepatitis C virus (HCV) is the aetiological agent responsible for most cases of non-A non-B hepatitis.Hepatitis C is a disease of clinical importance because of its high infection rate in blood donors and its persistence as chronic infections which may lead to cirrhosis and hepatocellular carcinoma in the long term. The variability of the HCV genome has posed difficulties in serological detection and vaccine design. The recent advance in phage technology offers a means of cloning human anti-HCV antibodies of a defined specificity that may have potential therapeutic use. We now report the generation of a phage display library using the V H genes of a HCV-infected patient and the V L genes of two non-immune individuals. From this library we were able to obtain specific IgG single-chain Fvs (scFvs) that recognize viral core and envelope proteins by selection on synthetic peptides derived from the core sequence PKARRPEGRTWAQPG and the envelope E2 sequence RPIDDFDQGWGPITY. The specificity of the scFvs was demonstrated by their specific reactions with homologous peptides in ELISA and the specific blocking of scFv binding by homologous peptides, in a dose-dependent manner, in inhibition ELISA. The binding of the anticore 4c2 to homologous peptide was blocked by HCV-positive human sera in an antibody-concentration-dependent manner, suggesting that the scFv recognizes a similar if not identical epitope to those of one or more of the polyclonal antibodies present in the sera.

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A proposed system for the nomenclature of hepatitis C viral genotypes

Cited by 903 publications

References 21 publications

Variation of the hepatitis C virus 5' non-coding region: implications for secondary structure, virus detection and typing

Variation of the hepatitis C virus 5' non-coding region: implications for secondary structure, virus detection and typing

Intrahepatic hepatitis C RNA levels do not correlate with degree of liver injury in patients with chronic hepatitis C

Human recombinant antibodies specific for hepatitis C virus core and envelope E2 peptides from an immune phage display library

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