Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The gene encoding the spike glycoprotein (S) of bovine enteric coronavirus (BECV) was cloned and its complete sequence of 4092 nucleotides was determined. This sequence contained a single long open reading frame with a coding capacity of 1363 amino acids (Mr 150,747). The predicted protein had 19 N-glycosylation sites. A signal sequence comprising 17 amino acids was observed starting from the first methionine residue. A potential peptidase cleavage site was located between amino acids 763 and 767. These cleavage explain the maturation of the primary product of the S gene to S1 (Mr 104,692) and S2 (Mr 84,175) spike structural proteins. Two amphipathic alpha-helices (amino acids 1007 to 1077 and 1269 to 1294) which may constitute the 12 nm stalk of the viral spike were also observed; another alpha-helix (amino acids 1305 to 1335) may be involved in the anchorage of the spike in the viral membrane. Comparison of this protein sequence to the described homologous mouse hepatitis (MHV) strain A59 and MHV-JHM S protein sequences led us to suggest that MHV-A59 and MHV-JHM S genes could be derived from a deletion of the BECV S gene.
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PMID:Nucleotide sequence of the glycoprotein S gene of bovine enteric coronavirus and comparison with the S proteins of two mouse hepatitis virus strains. 215

Liver disease in pregnancy is uncommon, acute viral hepatitis being the most frequent. The latter has a normal prognosis in pregnancy, with the possible exception of NANB hepatitis in India and North Africa. Immunization of neonates born of mothers suffering from acute or chronic HBV is essential and effective. Acute fatty liver of pregnancy has a better prognosis than previously thought, perhaps due to diagnosis of milder cases or improved intensive care. Its etiology is still unknown, but metabolic stress may be important. The confusion and overlap of AFLP, the HELLP syndrome, and liver disease of eclampsia suggest common etiological factors. Urgent delivery of the fetus is recommended in AFLP. The related condition of acute liver rupture may be diagnosed by ultrasound. Successful conservative management has been reported. Estrogens are involved in the pathophysiology of ICP, but this does not explain the profound racial differences in incidence. The nature of the sensitivity to estrogens is not understood, although reduced membrane fluidity, which may be counteracted by S-adenosyl-L-methionine, is one possible explanation. The increased fetal loss associated with ICP suggests that treatment should be more energetic than hitherto. In the worst affected individuals, fetal malnutrition secondary to maternal steatorrhea may be an important factor. In general, patients with chronic liver disease have increased maternal and particularly fetal mortality.
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PMID:Diagnosis and management of liver disease in pregnancy. 240 96

To determine which of the major ground squirrel hepatitis virus RNAs serve as mRNAs and which serve as templates for reverse transcription of the genome, we analyzed the subcellular distribution of these RNAs in livers of infected ground squirrels. Both major classes of viral RNA, the 2.3- and 3.5-kilobase (kb) classes, are unspliced, are polyadenylated at a common position, and display heterogeneous 5' ends that can encode proteins with different amino termini (G.H. Enders, D. Ganem, and H. Varmus, Cell 42:297-308, 1985). Both of the 2.3-kb RNAs, which encode surface antigens, appear to be predominantly associated with polyribosomes. Of the three 3.5-kb RNAs, the two longer, which can encode a protein initiated from the first methionine codon in the core antigen gene, appear to be predominantly associated with polyribosomes, and a minority of the shortest 3.5-kb RNAs, which can encode a protein initiated from the second methionine in the core antigen gene, appears to be associated with polyribosomes. This last RNA is instead found predominantly within viral core particles, consistent with evidence that indirectly implicates it in two steps of viral DNA synthesis (C. Seeger, D. Ganem, and H.E. Varmus, Science 232:477-484, 1986). None of the other viral RNAs is detectably packaged into cores. These findings provide independent evidence that the shortest 3.5-kb RNA is the template for synthesis of the viral genome and reveal a novel selectivity in viral RNA packaging.
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PMID:5'-terminal sequences influence the segregation of ground squirrel hepatitis virus RNAs into polyribosomes and viral core particles. 243 Nov 65

On the basis of the complete nucleotide sequence of the single-stranded, covalently closed circular hepatitis delta virus RNA genome (K.-S. Wang, Q.-L. Choo, A. J. Weiner, J.-H. Ou, R. C. Najarian, R. M. Thayer, G. T. Mullenbach, K. J. Denniston, J. L. Gerin, and M. Houghton, Nature [London] 323:508-514, 1986 [Author's correction, 328:456, 1987]), five long open reading frames (ORFs) encoding polypeptides containing a methionine proximal to the amino terminus were expressed in bacteria. Only polypeptides encoded by the antigenomic ORF5 cross-reacted with antisera obtained from patients with hepatitis delta virus infections. Immunological analysis of viral extracts and the recombinant ORF5 polypeptides synthesized in bacteria and yeast cells revealed that ORF5 encodes the immunogenic epitope(s) shared by both hepatitis delta viral polypeptides p27 delta and p24 delta and probably represents the complete structural gene for p27 delta and p24 delta. We also present evidence that ORF5 encodes the hepatitis delta antigen, an antigen originally found in the nuclei of hepatocytes of infected individuals (M. Rizzetto, M. G. Canese, S. Arico, O. Crivelli, F. Bonino, C. G. Trepo, and G. Verme, Gut 18:997-1003, 1977). A comparison of the primary structure of the predicted hepatitis delta antigen polypeptides with that of the core antigen of the hepatitis B virus shows that these polypeptides are very dissimilar.
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PMID:A single antigenomic open reading frame of the hepatitis delta virus encodes the epitope(s) of both hepatitis delta antigen polypeptides p24 delta and p27 delta. 244 91

In order to clone hepatitis C (blood-borne non-A, non-B hepatitis) virus, lambda gt11-cDNA library was constructed from RNA extracted from 100 liters serum collected from 1,047 donors with elevated ALT levels and negative for hepatitis B virus-DNA. The library was immunoscreened on Y1090 cells with pooled serum obtained from patients with acute hepatitis C or chronic hepatitis C. By screening 29 clones specific for Japanese hepatitis C infection were isolated. The specificity of these clones for hepatitis C infection was determined by panels constructed in 3 laboratories. Of these, 12 clones were specific for American hepatitis C infection as well. The nucleotide sequence (201 bp) of one of them was determined to be unique compared to known human viruses including hepatitis A virus, hepatitis B virus and hepatitis D virus. Southern blot analysis showed the absence of the sequence of the human genome in the clone. The predicted amino acid sequence is rich in residues of lysine, arginine, glutamic acid and asparagine, while lacking leucine, cysteine and methionine.
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PMID:Cloning of a cDNA associated with acute and chronic hepatitis C infection generated from patients serum RNA. 250 78

Monolayers of suckling rat hepatocytes cultured for 24 hours were treated with galactose, I-tyrosine and I-methionine. The purpose was to study the reasons for the clinical improvement of patients with neonatal hepatitis after dietary restriction of these nutrients. Galactose, tyrosine, and methionine was cytotoxic on suckling rat hepatocytes, yet had no effect on adult rat hepatocytes. Furthermore, the pretreatment of suckling rat hepatocytes with dexamethasone ameliorated the cytotoxicity and induced a differentiation of the cells. These results suggested that the cytotoxicity resulted from the immaturity of suckling rat hepatocytes and therefore dietary restriction of galactose, tyrosine and methionine might be a useful treatment for patients with neonatal hepatitis.
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PMID:Cytotoxicity of galactose, tyrosine and methionine in cultured suckling rat hepatocytes: relation to liver immaturity. 260 21

A study was conducted to estimate the functional reserve of the liver of patients with severe hepatitis by computed tomography (CT), in particular employing the integrated CT number of the whole liver (ICTN). ICTN was calculated by integrating the product of "area" times "mean CT number" of the liver in each CT slice for the entire height of the liver. The following results were obtained: 1) In patients with fulminant hepatitis (FH) as well as those with subacute hepatitis (SAH), ICTN was found to be significantly lower as compared to that of patients with acute hepatitis (AH) or non-hepatic diseases. In addition, in FH and SAH patients, ICTN showed a larger degree of decrease when compared with such conventional parameters as either estimated liver volume or mean hepatic CT number. Thus, ICTN seems to more sensitively reflect the changes in functional reserve of the liver. 2) ICTN showed significant positive correlations with prothrombin time and plasma BCAA/AAA ratio, and a significant negative correlation with plasma methionine level. 3) Time course of changes in ICTN correlated well with the clinical features of severe hepatitis. In particular, patients with initial ICTN values above 20 l.HU/m2 of body surface area showed significantly higher survival rate than those with initial ICTN below 20. In conclusion, ICTN well indicates the functional reserve of the liver, and is further suggested to be valuable as a parameter to predict the prognosis of patients with severe hepatitis.
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PMID:Determination of the integrated CT number of the whole liver in patients with severe hepatitis: as an indicator of the functional reserve of the liver. 274 45

The results of the experiments with use of isoniazid and its metabolites showed that in the liver of rats isoniazid induced albuminous degeneration with stroma inflammation and hepatocyte necrosis, monoacetylhydrazine induced fatty hepatosis, acetylisoniazid induced fatty hepatosis with stroma inflammation and hepatocyte necrosis and isonicotinic acid induced granular degeneration. Piracetam proved to be efficient in fatty hepatosis. Riboxin and dibunol were efficient in hepatitis. The drugs used clinically as liver protectors, i.e. cobamamide, pyridoxal phosphate and methionine had no protective action in liver affections induced by isoniazid whereas catergen, lipamide, dipromonium and methindione even aggravated such affections.
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PMID:[Drug prophylaxis of liver lesions induced by isoniazid and its metabolites]. 274 56

We have defined three categories of cultured cell lines on the basis of their permissiveness (susceptibility to initial infection) to mouse hepatitis virus (MHV). Fully permissive L-2 cells gave rise to 100-1000-fold higher numbers of infectious centers than did semi-permissive LM, LM-K or C-1300 cells, whereas non-permissive Vero or C-6 cells were refractory to MHV infection. On an infected cell basis, there was no deficiency on the part of semi-permissive cell lines to replicate total viral RNA, viral polypeptides or progeny virions. Two of the semi-permissive cell lines (LM and LM-K) supported persistent MHV infection, while a third (C-1300) succumbed to lytic infection. LM and LM-K cells, but not C-1300 cells showed resistance to MHV-induced membrane fusion, even when placed in contact with fusion-active MHV-infected L-2 cells. The ability of a given cell to undergo fusion did not correlate with membrane lipid characteristics (unsaturated fatty acid and sterol content) which contribute to membrane "fluidity". In order to more closely study the parameters of MHV-induced cell fusion, membranes were prepared from MHV-infected L-2 cells and monitored for their fusogenic potential with permissive L-2 cells, semi-permissive LM cells and non-permissive vero cells. Fusion was only observed with the permissive L-2 cells, and only when exogenous protease (trypsin or chymotrypsin) was added. When the membranes were prepared from 35S-methionine-labeled MHV-infected L-2 cells and subjected to protease treatment, the radiolabeled 180,000 dalton form of the E2-glycoprotein underwent proteolytic cleavage to yield a major product of approximately 90,000 daltons. Both trypsin and chymotrypsin were effective in this proteolytic cleavage and in activating membrane fusion. In a normally permissive, fusogenic infection of MHV in L-2 cells, the protease inhibitors TPCK and ZPCK, but not TLCK, were found to inhibit cell fusion. In MHV-infected L-2 cells, E2 was found almost exclusively as the 180,000 dalton form but turned over rapidly as shown by pulse-chase studies. TPCK and ZPCK but not TLCK inhibited turnover. The results suggest that L-2 cells contain a protease which cleaves at aromatic amino acids such as phenylalanine, and that this protease cleaves the 180,000 dalton form of the E2 to peptide fragments, one or more of which may activate cell fusion.
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PMID:The role of protease-dependent cell membrane fusion in persistent and lytic infections of murine hepatitis virus. 282 27

Infection of mouse L-2 fibroblasts with mouse hepatitis virus (MHV) results in strong inhibition of host cell protein synthesis. Since it has been suggested in other virus systems that translational control is modulated by changes in the intracellular ionic environment, we investigated the possible occurrence of similar changes during MHV infection. Membrane permeability to extracellular sodium ions was measured by culturing MHV-infected cells in the presence of 22Na+. Sodium influx into MHV-infected cells rose dramatically from 4 to 6 h post-infection. This influx correlated chronologically with the expression of MHV-mediated cell fusion. Cell fusion was blocked by the addition of a monoclonal antibody against the MHV E2 glycoprotein. This addition also resulted in a reduction in the normal influx of 22Na+, suggesting that E2 expression was responsible, directly or indirectly, for the increased permeability to sodium ions in infected cells. Cultures of MHV-infected cells were labelled with [35S]methionine in the presence of medium supplemented with sodium chloride at final concentrations ranging from 150 mM to 350 mM. Incorporation of radiolabel into proteins decreased with increasing NaCl concentration; however, the ratio of viral to cellular protein synthesis remained relatively constant. Similarly, alteration of intracellular Na+ and K+ levels by treatment of infected cells with ouabain had little effect on the pattern of viral/cellular protein synthesis. Using monoclonal anti-E2 antibody to inhibit Na+ influx, we demonstrated normal inhibition of host cell protein synthesis. We therefore conclude that MHV-induced shut-off of host translation is not mediated by changes in intracellular Na+ concentrations.
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PMID:Translational regulation in mouse hepatitis virus infection is not mediated by altered intracellular ion concentrations. 303 44


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