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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By means of a radioimmunoassay a substance excreted in feces could be detected in patients with hepatitis non-A,non-B (HNANB). Feces extracts of patients with sporadic and posttransfusion HNANB as well as of healthy persons were precipitated with PEG, digested with RNase and DNase and separated on CsCl. In HNANB-patients a RIA-positive material with a density of 1.3 g/ml CsCl could be detected which contained a partially double-stranded circular DNA. Cloning of this DNA in lambda-phase resulted in DNA of about 5 Kb, which hybridized with feces DNA under stringent conditions. The 5 Kb-DNA were mapped with different restriction enzymes. A 1.5 Kb EcoRi-fragment cross-hybridizes with HBV-DNA. No hybridization and sequence homologies were found with human, viral and procaryotic DNA as well as with plasmid and phage DNA (data base EMBL, Heidelberg). It is assumed that the DNA excreted in feces of HNANB-patients represents a viral genome not detected so far.
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PMID:[A hepatitis non-A, non-B-associated substance in the feces--identification and cloning of a partially double-stranded circular DNA]. 284 Dec 37

A human agent of non-A, non-B hepatitis (Inoculum I) was transmitted to chimpanzees and alterations in liver and lymphocytes were studied by electron microscopy and by cytochemical techniques during the acute phase of the disease. Three types of cytoplasmic alterations, consisting of a membraneous and an amorphous part were observed in the hepatocytes. The density of the amorphous constituent decreased after treatment with pronase, but not after treatment with ribonuclease (RNase) or deoxyribonuclease (DNase). The wall of C-III, but not C-II had fibrils with a periodicity the contrast of which markedly increased after pronase treatment. Cytochemical data suggest that the inclusions (C-I-III) represent a cellular reaction to the infectious agent rather than the virus itself. Intranuclear vermicular inclusions (INI) were observed in hepatocytes and lymphocytes as well, mainly in degenerating cells. Tubuloreticular inclusions (TRS) did not appear in circulating lymphocytes during acute infection; however, they could be induced by human alpha interferon treatment in vitro. Increased numbers of lymphocytes with parallel tubular arrays (PTA) were noted at the peak of serum aminotransferase elevations. The latter two alterations (TRS and PTA) most likely represent immunologic reactions of the host to the infectious agent.
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PMID:Ultrastructural and cytochemical study of hepatocytes and lymphocytes during experimental non-A, non-B infections in chimpanzees. 393 94

Australia antigen [Au(1)], a particle associated with viral hepatitis, was isolated from the plasma of a patient with chronic anicteric hepatitis and leukemia who had received radioactive phosphorus. We have found that the immunoreactivity and appearance of Au(1) in the electron microscope were not altered by treatment with enzymes including trypsin, pronase, lipase, phospholipase C, ribonuclease, deoxyribonuclease, amylase, and neuraminidase. In contrast, other serum constituents were degraded by these enzymes. Therefore, treatment of the patient's plasma with many enzymes was exploited as an initial step for the isolation of Au(1). Subsequently, Au(1) was purified from the enzyme-treated (32)P-labeled plasma by gel filtration through Sephadex G-200 and centrifugation through sucrose and in cesium chloride gradients. There were no detectable human serum components in the purest fractions, as tested by immunoelectrophoresis and immunodiffusion. The density of the purified Au(1) was 1.21 in CsCl. The particle measured about 200 A in diameter, was predominantly spherical in shape and appeared to be composed of subunits. Nucleic acids were not detected by spectrophotometric, radiochemical, and chemical analyses. Immunoreactivity of purified Au(1) was destroyed by heating for 1 hr at 85 degrees C but was stable at 56 degrees C. Treatment with Carnoy's solution (3 parts ethanol:1 part glacial acetic acid) followed by pronase disrupted the particles as seen with the electron microscope. These findings, combined with other published information on Australia antigen and viral hepatitis, suggest that the bulk of Australia antigen in the blood of this patient is an incomplete virus or virus capsid.
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PMID:Australia antigen (a hepatitis-associated antigen): purification and physical properties. 424 40

Physico-chemical and biological properties of an interferon inducer, a natural double-stranded RNA (dsRNA) obtained from RNA-genome bacteriophage-infected E. coli are described. Three independent methods i.e. sedimentation analysis, gel chromatography, and direct measurement of electronograms, were used to determine an average length of dsRNA molecules which was found to correspond to about 432 nucleotide pairs. dsRNA melting temperature in 0.15 M NaCl is 103 degrees C, and the resistance to RNase A is above 85%. Additional purification of the preparation by the methods eliminating bacterial endotoxin and other possible admixtures does not decrease acute toxicity of dsRNA. The influence of dsRNA on the cytolytic activity of natural killers (NK) in normal subjects and patients with viral diseases of the liver was demonstrated. dsRNA enhances the activity of NK in normal subjects as well as in patients with acute virus hepatitis B in the abatement stage of the disease and in patients with chronic persisting hepatitis. At the peak of acute virus hepatitis B NK stimulation was detected in only 40 +/- 16% of the patients. In patients with chronic active liver diseases dsRNA enhanced NK activity in 50 +/- 22% of cases. A similar effect on NK cell activity is exerted by human leukocyte interferon.
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PMID:[Physicochemical and biological properties of double-stranded RNA--an interferon inducer]. 620 91

The ribonucleoprotein (RNP) of avian infectious bronchitis virus (IBV) was examined by electron microscopy after shadowing with carbon/platinum. Linear RNP strands up to 6.7 microns in length, from three IVB strains, were sensitive to both pancreatic RNase and to proteases. These strands were obtained from spontaneously disrupted complete particles but not from disrupted incomplete particles that lacked RNP. They were also released from Nonidet P40-disrupted particles and could be isolated on sucrose density gradients at a density of 1.27 g/ml. In some cases, helical RNP complexes associated with virus particles were observed that were similar to RNPs of human coronavirus strain 229E and mouse hepatitis virus strain 3.
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PMID:Ribonucleoprotein of avian infectious bronchitis virus. 626 41

We have shown by T(1) oligonucleotide fingerprinting that the genome of mouse hepatitis virus strain A59 and its intracellular RNA 1 have identical fingerprints and that RNA 1 and the subgenomic RNAs 3, 6, and 7 contain common sequences. To localize the homologous region between the RNAs, we compared fingerprints of the 3' terminus of the genome with those of RNA 7. The genome was partially degraded with alkali, and polyadenylate-containing fragments were purified by oligodeoxythymidylate-cellulose chromatography. The fragments were size fractionated by agarose-urea gel electrophoresis, and two pools, x and z, containing 3'-derived fragments of the genome with apparent molecular weights of 0.1 x 10(6) to 0.14 x 10(6) and 0.6 x 10(6) to 0.8 x 10(6), respectively, were further analyzed by RNase T(1) oligonucleotide fingerprinting. Comparison of the fingerprints of RNAs 6 and 7 with those of pools x and z showed that these subgenomic RNAs extend inwards from the 3' terminus of the genome. The RNA fragments present in pool z were on average slightly larger than RNA 7 as confirmed by the presence in pool z of T(1) oligonucleotide spots specific for RNA 6 but not present in RNA 7. However, two large oligonucleotide spots derived from RNA 7, which were also present in RNAs 1, 3, and 6 and in the virion RNA, were not found in the T(1) oligonucleotide map of pool z. A possible explanation is that the two spots were derived from a leader sequence. The results of UV transcription mapping experiments (L. Jacobs, W. J. M. Spaan, M. C. Horzinek, and B. A. M. van der Zeijst, J. Virol. 39:401-406, 1981) excluded the possibility that such a leader sequence arises by splicing from a larger precursor molecule, but either a virus-specific RNA primer molecule for the synthesis of mRNAs or an RNA polymerase jumping mechanism could explain the presence of a leader sequence.
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PMID:Sequence relationships between the genome and the intracellular RNA species 1, 3, 6, and 7 of mouse hepatitis virus strain A59. 628 66

There are seven virus-specific mRNA species in mouse hepatitis virus-infected cells (Lai et al., J. Virol. 39:823-834, 1981). In this study, we examined virus-specific negative-stranded RNA to determine whether there are corresponding multiple negative-stranded RNAs. Intracellular RNA from mouse hepatitis virus-infected cells was separated by agarose gel electrophoresis, transferred to nitrocellulose membranes, and hybridized to positive-stranded genomic 60S [32P]RNA. Only a single RNA species of genomic size was detected under these conditions. This RNA was negative stranded. No negative-stranded subgenomic RNA was detected. We also studied double-stranded replicative-form RNA in the infected cells. Only one replicative-form of genomic size was detected. When the double-stranded RNA isolated without RNase treatment was analyzed, again only one RNA species of genomic size was detectable. Furthermore, most of the virus-specific mRNAs could be released from this RNA species upon heating. These results suggest that all of the mouse hepatitis virus-specific RNAs are transcribed from a single species of negative-stranded RNA template of genomic size.
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PMID:Replication of mouse hepatitis virus: negative-stranded RNA and replicative form RNA are of genome length. 629 13

Mouse hepatitis virus A59 codes for seven mRNAs in infected cells. These mRNAs are transcribed from a minus (-) strand template of genome length and contain a leader RNA at their 5' ends. To further elucidate the mechanism of coronavirus transcription, we examined the structure of mouse hepatitis virus replicative intermediates (RIs) isolated by 2 M NaCl precipitation and Sepharose 2-B column chromatography. Purified RIs migrated as a single species on agarose gels and sedimented between 12 and 38S on 10 to 25% sucrose gradients. The complexes were readily heat denatured into a heterogeneous population of smaller RNA molecules which probably represent nascent plus (+) strands. RNase A digestion of RIs produced a single replicative form which sedimented between 30 and 32S. These data suggest that the RI is composed of a single genome-sized (-) strand hydrogen bonded to an average of 4 to 6.5 nascent (+) strands. In contrast, a column-purified replicative form was extremely resistant to RNase A digestion and heat denaturation and migrated as a single RNA species on agarose gels and sucrose gradients. Oligonucleotide fingerprinting of an RI revealed the presence of the 5' leader RNA on the nascent (+) strands. In addition, an average of 6.2 cap structures were present in each RI, which agrees with the average number of nascent (+) strands per RI. These data suggest that the leader RNA is utilized as a primer for mouse hepatitis virus RNA transcription and is not added to mRNA post-transcriptionally.
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PMID:Characterization of replicative intermediate RNA of mouse hepatitis virus: presence of leader RNA sequences on nascent chains. 631 63

The mouse biliary glycoprotein 1 gene (bgp1) encodes several multifunctional glycoprotein isoforms. These glycoproteins represent members of the carcinoembryonic antigen (CEA) family which belongs to the immunoglobulin superfamily. The Bgp1 glycoproteins function as cell adhesion molecules and receptors for the mouse hepatitis viruses. In contrast to CEA, whose overexpression has been correlated with cancer progression, the human and mouse Bgp proteins are generally down-regulated upon tumor formation. In this study, we report on the mouse bgp1 gene organization and transcriptional activation. We have isolated phage and cosmid clones encompassing the entire bgp1 coding region. This gene consists of nine exons, some of which are subjected to alternative splicing producing a minimum of four splice variants. A comparison of the murine bgp1 proximal promoter with the human BGP and mouse cea10/bgp3 genes revealed sequence conservation of 66% and 95%, respectively. RNase protection assays and primer extension analyses indicated that the mouse bgp1 transcriptional start site is positioned 240 nucleotides upstream of the ATG translational initiation codon, which is 140 nucleotides further upstream than in any other CEA family member. The bgp1 promoter is transcriptionally active in reporter gene activation in vitro transfection studies and in vivo using a bgp1-containing cosmid clone. We identified three putative AP-2 or AP-2-like sites and an upstream stimulatory factor (USF) recognition sequence within the proximal mouse bgp1 promoter region at positions similar to those used by the human BGP promoter region. These data suggest that the regulation of the mouse and human BGP genes may follow some common spatial and temporal expression. Interestingly, the bgp1 proximal promoter and coding region are also well conserved throughout evolution.
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PMID:Characterization and transcriptional activity of the mouse biliary glycoprotein 1 gene, a carcinoembryonic antigen-related gene. 762 60

Although the hepatitis delta virus genome contains multiple open reading frames, only one of these reading frames is known to be expressed during replication of the virus. This open reading frame encodes two distinct molecular species of hepatitis delta antigen (HDAg), p24 delta and p27 delta, depending on the location of the stop codon which terminates translation. We found antibody specific for p27 delta to be capable of precipitating p24 delta in extracts of infected liver, indicating that p27 delta and p24 delta form heterologous complexes in vivo. After cross-linking with 0.05% glutaraldehyde, specific HDAg dimers were detected in antigen prepared from both the liver and serum of an HDV-infected woodchuck carrier of woodchuck hepatitis virus. Guanidine HCl-denatured HDAg extracted from liver and dialyzed against phosphate-buffered saline sedimented in rate-zonal sucrose density gradients as 15S multimeric complexes. These 15S multimers were stable in the presence of 1.2% Nonidet P-40. After RNase digestion, the 15S complex was reduced to a 12S complex without associated RNA, while boiling for 3 min in 1% sodium dodecyl sulfate-0.5% 2-mercaptoethanol further reduced the 15S complex to 3S HDAg monomers. In the absence of glutaraldehyde cross-linking, HDAg extracted from liver migrated as monomer species in reducing and nonreducing gels, suggesting that the conserved cysteine residue present in p27 delta does not play a role in the formation of either dimers or multimers. On the other hand, an amino-terminal chymotrypsin-digested HDAg fragment, with a predicted length of 81 or less amino acids, retained the ability to form dimers, consistent with the hypothesis that a coiled-coil motif present between residues 27 and 58 may play a role in HDAg protein interactions in vivo.
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PMID:Hepatitis delta virus antigen forms dimers and multimeric complexes in vivo. 767 57


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