Non-A, Non-B Hepatitis in Chimpanzees and Marmosets

Feinstone, S. M.; Alter, Harvey J.; Dienes, Hans Peter; Shimizu, Yohko K.; Pópper, Hans; Blackmore, D.K.; Sly, D. L.; London, William T.; Purcell, Robert H.

doi:10.1093/infdis/144.6.588

Cited by 196 publications

(127 citation statements)

References 26 publications

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“…Plasma was collected over a 13-year period from patient H who developed chronic, posttransfusion NANB hepatitis in 1977 (18). Recent investigation indicates that the etiological agent of the NANB hepatitis infection was HCV (P. Farci, H.J.A., and R.H.P., unpublished data).…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Nucleotide sequence and mutation rate of the H strain of hepatitis C virus.

Ogata

Alter

Miller

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

555

343

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Patient H is an American patient who was infected with hepatitis C virus (HCV) in 1977. The patient became chronically infected and has remained so for the past 13 years. In this study, we compared the nucleotide and predicted amino acid sequences of the HCV genome obtained from plasma collected in 1977 with that collected in 1990. We find that the two HCV isolates differ at 123 of the 4923 (2.50%) nucleotides sequenced. We estimate that the mutation rate of the H strain of HCV is -1.92 x 10-3 base substitutions per genome site per year. The nucleotide changes were exclusively base substitutions and were unevenly distributed throughout the genome. A relatively high rate of change was observed in the region of the HCV genome that corresponds to the nonstructural protein 1 gene region of flaviviruses, where 44 of 960 (4.6%) nucleotides were different. Within this region there was a 39-nucleotide domain in which 28.2% of the nucleotides differed between the two isolates. In contrast, relatively few nucleotide substitutions were observed in the 5' noncoding region, where only 2 of 276 (0.7%) nucleotides were different. Our results suggest that the mutation rate of the HCV genome is similar to that of other RNA viruses and that genes appear to be evolving at different rates within the virus genome.

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Section: Resultsmentioning

confidence: 99%

“…Patient H is an American with chronic posttransfusion NANB hepatitis (18). The plasma samples under study were obtained on July 12, 1977 (i.e., at the early acute stage of infection) and on August 1, 1990, which represents an interval of 13 years of continuous replication of the virus (P. Farci, H.J.A., and R.H.P., unpublished results).…”

Section: Methodsmentioning

confidence: 99%

Nucleotide sequence and mutation rate of the H strain of hepatitis C virus.

Ogata

Alter

Miller

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

555

343

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“…A cDNA clone of the HCV genome was generated from the liver of a chimpanzee infected with the H strain of HCV (Feinstone et al, 1981). Briefly, RNA purified by caesium trifluoroacetate isopycnic centrifugation (Zarlenga & Gamble, 1987) was used as a template for cDNA synthesis (Giibler & Hoffman, 1983) with primers based on the published HCV cDNA sequence (Choo et al, 1991).…”

Section: Molecular Cloning Of the Hcv Genomementioning

confidence: 99%

Processing of the E1 glycoprotein of hepatitis C virus expressed in mammalian cells

Fournillier-Jacob

Cahour²,

Escriou³

et al. 1996

Journal of General Virology

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The structural part of the hepatitis C virus (HCV) genome encodes a capsid protein, C, and two envelope glycoproteins, E1 and E2, released from the virus polyprotein precursor by signalase(s) cleavage(s). The processing of E1 was investigated by infecting simian cells with recombinant vaccinia viruses expressing parts of the HCV structural proteins. When the predicted E1 sequence was expressed alone (amino acid residues 174-370 of the polyprotein) or with the capsid protein gene (residues 1-370), it showed an apparent molecular mass of 35 kDa as measured by SDS-PAGE analysis. However, when E1 was expressed as part of a truncated C-El-truncated E2 polypeptide (residues 132-383), the processed E1 product had the expected apparent molecular mass of 31 kDa, suggesting that flanking sequences are necessary for the generation of the mature 31 kDa E1 form. The N-terminal sequence of the two E1 forms was found to be the same. Analysis of the glycosylation pattern showed that, in both species, only four of the five potential N-linked glycosylation sites were recognized, indicating that glycosylation was not involved in the molecular mass difference. We showed that expression of E1 with or without the hydrophobic stretch of amino acids residues 371-383, defined as the E2 signal sequence, may be responsible for the difference in electrophoretic mobility of the two E1 species. In vitro translation assays and site-directed mutagenesis experiments suggest that this sequence remains part of the 31 kDa E1 mature protein.

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“…In some experiments, human plasma H, containing 1065 50o chimpanzee infectious doses (CID50) per ml of HCV (12) Nucleic acids present in 100 /xl of HCV-containing serum or normal serum were also processed. Liver RNA was isolated by the guanidinium thiocyanate/cesium chloride method (16).…”

mentioning

confidence: 99%

“…Selected experiments were repeated with the wellcharacterized H-strain of HCV (12). A 2.25-ml sample of cell suspension containing 1.5 x 106 MOLT-4 Ma cells was inoculated with 0.25 ml of plasma containing HCV, strain H. In this experiment fresh MOLT4 Ma cells were added to the cultures at 2-to 5-day intervals in an attempt to maintain the positive cultures longer.…”

mentioning

confidence: 99%

Evidence for in vitro replication of hepatitis C virus genome in a human T-cell line.

Shimizu

Iwamoto

Hijikata

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

305

169

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A human T-cell line, MOLT-4, either uninfected or infected with murine retroviruses, was tested for its susceptibility to hepatitis -C virus (HCV) infection. The cell cultures were inoculated with a serum containin HCV and then examined for the presence of viral sequences by cDNA/PCR. In murine retrovirus-infected MOLT-4 (MOLT-4 Ma) cells, intracellular minus-strand viral RNA, a putative replication intermediate, was first detected 3 days after inoculation, and the maximum signal was seen on day 7. When the cells were continuously subcultured in fresh medium, HCV sequences were intermittently detected in cells over a period of 3 weeks. In MOLT-4 cells free of retroviruses, replication of minus-strand HCV RNA appeared less efficient than in MOLT-4 Ma cells. The presence of minus-strand viral RNA in MOLT-4 Ma cells inoculated with HCV was confirmed by in situ hybridization with a strand-specific RNA probe. Immunofluorescence tests with antibodies specific for HCV core and NS4 antigeus showed that MOLT-4 Ma cells were positive for viral antigen 7 days after inoculation. Thus, it appears likely that the HCV genome can replicate in the human T-cell line MOLT-4.

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Non-A, Non-B Hepatitis in Chimpanzees and Marmosets

Cited by 196 publications

References 26 publications

Nucleotide sequence and mutation rate of the H strain of hepatitis C virus.

Nucleotide sequence and mutation rate of the H strain of hepatitis C virus.

Processing of the E1 glycoprotein of hepatitis C virus expressed in mammalian cells

Evidence for in vitro replication of hepatitis C virus genome in a human T-cell line.

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