Transmission of enteric non‐A, non‐B hepatitis virus in <i>Macaca mulatta</i>, monkeys by intraportal route: Subsequent passages of HEV virus

Gupta, Hema; Joshi, Y. K.; Varma, Anupam; Shenoy, Suchitra; Sriramchari, S.; Iyenger, B.; Tandon, B. N.

doi:10.1111/j.1440-1746.1990.tb01114.x

Cited by 12 publications

(9 citation statements)

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“…Experimental hepatitis E produced by HEV from Mexico [Ticehurst et al, 1992] and from Asian countries [Arankalle et al, 1995;Gupta et al, 1990;Jameel et al, 1992;Krawczinski et al, 1989;Tsarev et al, 1992;Vrati et al, 1992] has been extensively studied in monkeys. However, hepatitis E due to African HEV has been reported in only one monkey [Chatterjee et al, 1997].…”

Section: Introductionmentioning

confidence: 99%

Experimental African HEV infection in cynomolgus macaques (Macaca fascicularis)

et al. 1998

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Experimental infection with hepatitis E virus (HEV) from Africa has not been investigated. Our purpose was to study hepatitis E produced by HEV from Chad (North Africa) and to analyze the genetic sequence of the HEV obtained after animal passage. An HEV-containing fecal sample from Chad was intravenously inoculated in four cynomolgus macaques. When serum Alanine Amino Transferase (ALT) levels rose, open liver biopsy and bile aspiration were performed. In all the monkeys, an ALT rise occurred 25 to 32 days after inoculation and new anti-HEV was detected by Enzyme Immuno Assay (EIA). Hepatic histopathology was consistent with acute viral hepatitis. HEV was detected by polymerase chain reaction (PCR) in bile (3/4 animals) and feces (2/4 animals) and by imunoelectron microscopy (IEM) in the inoculum and one bile specimen. A genetic variant HEV was identified in one monkey. The Chad HEV produced hepatitis E with pathophysiologic and histopathologic findings similar to those observed with HEV from other geographic origins. A genomic variant HEV population was produced after one passage in a macaque.

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Section: Introductionmentioning

confidence: 99%

Experimental African HEV infection in cynomolgus macaques (Macaca fascicularis)

et al. 1998

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“…The genome contains three open reading frames (ORFs) with ORF2 encoding the putative major structural or capsid protein. The cloning of geographically distinct strains of HEV and synthesis of recombinant HEV proteins [Reyes et al, 1990;Ichikawa et al, 1991;Tam et al, 1991;Yarbough et al, 1991;Aye et al, 1992;Huang et al, 1992;Uchida et al, 1992;He et al, 1993;Li et al, 1994] along with the development of animal models for HE infection [Gupta et al, 1990;Bradley, 1992;Jameel et al, 1992;Tsarev et al, 1992Tsarev et al, , 1995Arankalle et al, 1993;Longer et al, 1993] have made it possible to study antigenic and immunogenic epitopes of HEV proteins. In addition, the expression of ORF2 and ORF3 proteins in E. coli and Baculovirus systems, and the production of synthetic peptides have led to the development of diagnostic assays He et al, 1993;Yarbough et al, 1993;Paul et al, 1994].…”

Section: Introductionmentioning

confidence: 99%

Amino-terminal epitopes are exposed when full-length open reading frame 2 of hepatitis E virus is expressed inEscherichia coli, but carboxy-terminal epitopes are masked

et al. 1997

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We constructed a panel of overlapping and non-overlapping fragments of cDNA derived from open reading frame 2 (ORF2) of hepatitis E virus (HEV) and fused to the gene encoding glutathione S-transferase (GST), from which proteins were expressed in Escherichia coli. IgG-specific immunoreactivity against each protein was measured by Western immunoblotting using sera from experimentally infected Rhesus macaques (Macaca mulatta) or from HEV-infected patients. Under these conditions, full-length ORF2 protein (GST-ORF2) was strongly reactive with acute-phase sera from either macaques or patients, but was poorly reactive with convalescent sera. Recombinant protein GST-ORF2.3, representing amino acids 1-110 of the 660 encoded by ORF2, demonstrated a pattern of reactivity largely indistinguishable from the full-length protein. Conversely, GST-ORF2.1, representing amino acids 394-660 of the ORF2 protein was strongly reactive with both acute- and convalescent-phase sera. Extension of GST-ORF2.1 towards the N-terminus led to a progressive loss of convalescent-phase reactivity, apparent with as few as 20 additional HEV-specific amino acids. Deletion of 40 or more amino acids from the N-terminus of ORF2.1 also led to reduced convalescent-phase reactivity, however a protein representing this "reactive" region, containing amino acids 394-473, was poorly reactive, suggesting that the convalescent-reactive epitopes are conformational. Expression of full-length ORF2 protein in E. coli therefore masks the convalescent-reactive epitopes within the C-terminal part of the protein, without affecting N-terminal, acute-reactive epitopes.

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“…In some cases, the presence of HEV in a sample has been demonstrated by transmission to animals (5,(11)(12)(13)(14)(15)(16)(17)(18)(19) but such transmission studies cannot be used for routine investigation. Until recently, the primary method available for characterization of virus shedding was immune electron microscopy (IEM) (for reviews, see refs.…”

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confidence: 99%

“…1-4). However, because the level of HEV in feces and bile is very low (5,(11)(12)(13)(14)(15)(16)(17)(18)(19), the sensitivity of IEM is inadequate for complete characterization of HEV infection. A more sensitive technique, detection of the virus genome by reverse transcription-polymerase chain reaction (RT-PCR), was used in this study to correlate the presence of HEV in serum, bile, and feces of an experimentally infected cynomolgus monkey with biochemical evidence of hepatitis and development of antibodies to HEV (anti-HEV).…”

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Characterization of a prototype strain of hepatitis E virus.

Tsarev

Emerson

Reyes

et al. 1992

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

268

208

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A strain of hepatitis E virus (SAR-55) implicated in an epidemic of enterically transmitted non-A, non-B hepatitis, now called hepatitis E, was characterized extensively. Six cynomolgus monkeys (Macaca fascicularis) were infected with a strain of hepatitis E virus from Pakistan. Reverse transcription-polymerase chain reaction was used to determine the pattern of virus shedding in feces, bile, and serum relative to hepatitis and induction of specific antibodies. Virtually the entire genome of SAR-55 (7195 nucleotides) was sequenced.Comparison of the sequence of SAR-55 with that of a Burmese strain revealed a high level of homology except for one region encoding 100 amino acids of a putative nonstructural polyprotein. Identification of this region as hypervariable was obtained by partial sequencing of a third isolate of hepatitis E virus from Kirgizia.

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Transmission of enteric non‐A, non‐B hepatitis virus in Macaca mulatta, monkeys by intraportal route: Subsequent passages of HEV virus

Cited by 12 publications

References 10 publications

Experimental African HEV infection in cynomolgus macaques (Macaca fascicularis)

Experimental African HEV infection in cynomolgus macaques (Macaca fascicularis)

Amino-terminal epitopes are exposed when full-length open reading frame 2 of hepatitis E virus is expressed inEscherichia coli, but carboxy-terminal epitopes are masked

Characterization of a prototype strain of hepatitis E virus.

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