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 prevalence of antibody to hepatitis C virus, evidence of previous or current infection with this agent of parenterally transmitted non-A, non-B hepatitis, was determined in 340 subjects residing in the United Kingdom. The antibody was detected in 3 per cent of unselected blood donors and in 60 per cent of patients with chronic post-transfusion non-A, non-B hepatitis. Evidence for infection was also found in 30 per cent of intravenous drug abusers, and in 75 per cent of haemophiliacs receiving commercial factor VIII concentrate. The infection is uncommon in renal units and amongst sexually promiscuous groups attending sexually-transmitted disease clinics. Although the seropositivity rate in primary biliary cirrhosis and chronic B and delta hepatitis was very low (0-2 per cent), in patients with autoimmune and alcoholic liver disease it was 14-16 per cent which, although lower than that quoted in studies from Spain and Italy, is considerably higher than would be expected by chance. The reason for the high incidence of non-A, non-B hepatitis in this latter group of patients is unclear.
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PMID:Hepatitis C virus antibodies in subjects with and without liver disease in the United Kingdom. 217 97

It has previously been shown that human hepatitis virus delta antigen has an RNA-binding activity (Chang et al., J. Virol. 62:2403-2410, 1988). In the present study, the specificity of such an RNA-protein interaction was demonstrated by expressing various domains of the delta antigen in Escherichia coli as TrpE fusion proteins and testing their RNA-binding activities in a Northwestern protein-RNA immunoblot assay and RNA gel mobility shift assay. Hepatitis delta virus (HDV) RNA bound specifically to the delta antigen in the presence of an excess amount of unrelated RNAs and a relatively high salt concentration. Both genome- and antigenome-sense HDV RNAs and at least two different regions of HDV genomic RNA bound to the delta antigen. Surprisingly, these two different regions of HDV genomic RNA could compete with each other for delta antigen binding, although they do not have common nucleotide sequences. In contrast, this binding could not be competed with by other viral or cellular RNA. Since both the genomic and antigenomic HDV RNAs had strong intramolecular complementary sequences, these results suggest that the binding of delta antigen is probably specific for a secondary structure unique to the HDV RNA. By expressing different subdomains of the delta antigen, we found that the middle one-third of delta antigen was responsible for binding HDV RNA. Neither the N-terminal nor the C-terminal domain bound HDV RNA. Binding between the delta antigen and HDV RNA was also demonstrated within the HDV particles isolated from the plasma of a human delta hepatitis patient. This in vivo binding resisted treatment with 0.1% sodium dodecyl sulfate and 0.5% Nonidet P-40. In addition, we showed that the antiserum from a human patient with delta hepatitis reacted with all three subdomains of the delta antigen, indicating that all of the domains are immunogenic in vivo. These studies demonstrated the specific interaction between delta antigen and HDV RNA.
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PMID:Characterization of hepatitis delta antigen: specific binding to hepatitis delta virus RNA. 220 Aug 84

2346 liver samples from 17 areas in China were investigated for intrahepatic hepatitis D antigen (HDAg) by direct enzyme-labelled technique. HDAg was detected in 167 out of 1764 samples of HBsAg positive individuals with the detection rate of 9.47%. Hepatitis D virus (HDV) infection existed in all the examined areas without any significant difference regarding HDAg detection rate. A relationship of intrahepatic HDAg to the pathologic type of the liver disease was observed. The HDAg detection rate in chronic liver diseases and severe hepatitis was higher than in other liver diseases. It suggested that HDV infection was associated with the progression and chronicity of the liver disease. Studies on the relationship between HDV infection and HBV replication showed that HBV replication might be suppressed by HDV infection. Both HDV and HBV, however, could replicate in the same hepatocyte simultaneously.
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PMID:A study on hepatitis D virus infection in liver tissues of patients with hepatitis B in China. 221 54

Hepatitis A virus is an enteric picornavirus. Its genome is a single stranded RNA molecule of positive-strand polarity of 7478 bases. This sequence codes for a polyprotein which is processed to give rise to viral proteins VP-1, VP-2, VP-3 and others. Hepatitis B virus, a major worldwide infectious and cancer promoting agent contains a DNA genome of 3226 base pairs that replicates by a reverse transcriptase via an RNA intermediate. Extensive sequencing and expression experiments have revealed four major genes named surface, core, polymerase and X which are coded in more than one reading frame. Furthermore, within a frame, proteins are expressed from multiple initiation codons resulting in several related products. The viral genome of hepatitis C virus (nonA-nonB), an elusive major infectious agent, has recently been cloned. This genome is a single positive-stranded RNA of at least 10,000 bases which codes for several antigens, some of them associated specifically with nonA-nonB hepatitis infections. The hepatitis D (delta) viral agent, an infectious agent requiring a hepadnarious for propagation, contains a covalently closed circular single-stranded RNA genome of 1167 nucleotides. This genome encodes the protein p24 and p27 that bind specifically to antisera from patients with chronic hepatitis D infections.
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PMID:Hepatitis A, B, C, D and E viruses: structure of their genomes and general properties. 222 69

Hepatitis delta virus (HDV) superinfection of woodchuck chronic carriers of woodchuck hepatitis virus (WHV) results in acute and chronic disease. The different courses of disease mimicked the outcome of human HDV superinfection, making woodchucks valuable models for clinical studies of HDV. Ten of 11 woodchuck chronic carriers of WHV superinfected with HDV developed acute HDV infection with markers of viral replication in the serum and liver. One animal (DW128) had no serological markers of acute HDV infection. Nine of 11 (82%) superinfected animals developed chronic HDV infection. An unusual course of chronic HDV infection occurred in one woodchuck (DW128): no serum markers of acute or chronic HDV infection appeared but HDV RNA was detected in the liver, indicating that chronic HDV infection can occur without serological markers.
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PMID:Different outcomes of chronic hepatitis delta virus infection in woodchucks. 225 30

To clarify the correlation of hepatitis D virus (HDV) infection and viral replication in liver diseases, the authors detected HDV RNA and serological HDV markers in serum from 285 patients with hepatitis B and 45 asymptomatic carriers of HBsAg. With dot blot hybridization, serum HDV RNA was detected in 8.8% (29/330) of the patients with HBV infection. The positive rate of HDV RNA in fulminant hepatitis was higher than that in benign hepatitis (15/74 vs 3/47, P less than 0.05). 10 of the 139 patients with chronic active hepatitis and 1 of the 6 cases with cirrhosis were positive for HDV RNA. However, all of the 19 cases with chronic persistent hepatitis and 45 asymptomatic carriers of HBsAg were negative fo, HDV RNA. Serological HDV markers, HDAgr anti-HD and IgM-anti-HD, were determined with ELISA. HDV RNA was detected in all of the serum samples with positive HDAg and/or IgM-anti-HD, in 15 of the 26 cases with positive-anti-HD and in 8 cases without HDV markers. Our results showed that 40 of the 330 patients with HBsAg were infected by HDV. This investigation suggests that HDV is one of the etiological factors for fulminant hepatitis and chronic active hepatitis.
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PMID:[Hepatitis D virus RNA in serum from patients with hepatitis B]. 226 30

A morphologic study with immunohistochemical detection of the viral antigens of hepatitis B and Delta was performed on 36 liver specimens from patients with delta positive chronic viral hepatitis B. Electron microscopy was performed in 9 cases. No light microscopic or ultrastructural features specific for hepatitis D were observed. Lymphocytic infiltration occurred more often close to hepatocytes containing either hepatitis Delta antigen or hepatitis B core antigen in the cytoplasm, suggesting an involvement of cellular immune mechanisms in chronic hepatitis D as well as in hepatitis B. The simultaneous expression of both HBcAg and Delta antigen in occasional specimens over longer time periods indicates the possible co-existence of both viruses without mutual inhibition.
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PMID:Immuno-light and electron microscopic features of chronic hepatitis D. 230 77

The pattern of the immunoglobulin M antibody to the hepatitis delta virus distinguishes acute from chronic hepatitis D. Expression of the immunoglobulin M antibody to the hepatitis delta virus is relatively weak and short-lived in self-limited hepatitis but strong and persistent in chronic forms. To study the nature of the immunoglobulin M antibody to the hepatitis delta virus in acute hepatitis D and in chronic hepatitis D, antibody-positive sera were submitted to rate zonal centrifugation to separate monomeric 7S from pentameric 19S immunoglobulin M antibodies. Sera were from 6 patients with acute self-limited hepatitis, 4 patients with chronic hepatitis D, and 6 patients with hepatitis D progressing to chronicity. The immunoglobulin M reactivity was measured by a specific immunoassay based on capture of mu-chains by anti-mu linked on a solid phase. Only 19S antibody was found in acute hepatitis D. In contrast, all patients with chronic hepatitis D circulated 7S antibody in addition to the 19S antibody. In patients with progressive hepatitis D, both the 7S and 19S antibody variants were present at the onset of the disease. The difference in the antibody response between acute hepatitis D and chronic hepatitis D is not only temporal and quantitative but also qualitative. The expression of 7S antibody seems to be an immunologic event specific for chronic hepatitis D.
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PMID:Monomeric (7S) immunoglobulin M antibodies to hepatitis delta virus in hepatitis type D. 233 96

Hepatitis B virus DNA and hepatitis D virus RNA, the most sensitive markers of hepatitis B and hepatitis D virus replication, were sought by molecular hybridization with radioactive probes in serial serum samples from 29 consecutive patients with HBsAg-positive fulminant hepatitis. Nineteen patients had evidence of hepatitis D virus infection, as assessed by the presence in serum of delta antigen, anti-delta antibodies, or both. Hepatitis B virus DNA was found in only two patients: one was a chronic HBsAg carrier with hepatitis D virus superinfection and the other had fulminant hepatitis caused by hepatitis B and hepatitis D coinfection. Hepatitis D virus RNA was detected in three patients: two with hepatitis B and hepatitis D coinfection and also in the HBsAg carrier with positive hepatitis B virus DNA and hepatitis D virus superinfection. None of 10 patients with hepatitis B virus infection alone had detectable viral nucleic acids in serum. Overall, viral nucleic acids were detected in the sera of 4 of the 29 patients (14%). Hepatitis D virus antigenemia did not indicate hepatitis D virus replication because hepatitis D virus RNA was not detected in 9 of 12 patients with hepatitis D virus antigen in their sera. The low frequency of viral replication found in fulminant hepatitis B or D may explain the low recurrence rate of viral hepatitis in patients with fulminant hepatitis who have received liver transplantations.
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PMID:Hepatitis B virus and hepatitis D virus replication in HBsAg-positive fulminant hepatitis. 236 84

Hepatitis delta antigen (HDAg) is the only known protein encoded by the hepatitis delta virus (HDV). Two HDAg species of different sizes have been detected in the sera and livers of the infected humans, chimpanzees, and woodchucks, even though only one RNA species was previously identified in most of the HDV strains. To study HDAg heterogeneity, we took advantage of the fact that a single base mutation at nucleotide 1015 (C to U), which results in an amber termination codon in the HDAg open reading frame (ORF), eliminates a unique Ncol restriction enzyme site. We screened various HDV cDNA clones and detected sequence heterogeneity of the HDAg-coding region on the basis of the presence or absence of the Ncol site. Five delta hepatitis patients were examined. In every patient, two types of HDAg-coding sequence were detected at nucleotide 1015: one which contains a C and results in an ORF encoding a delta antigen of 214 amino acids, and the other which possesses a U and results in an amber termination codon and a truncated HDAg species of 195 amino acids. The in vitro translation products of these two ORFs comigrated with the two HDAg species from the patient's plasma on SDS polyacrylamide gels. Polymerase chain reaction (PCR) amplification of the HDV RNA from some patients' sera and subsequent sequencing showed several additional mutations in the HDAg-coding region. These mutations are independent of the C or U nucleotide change at the site of the amber termination codon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heterogeneity of hepatitis delta antigen. 238 57


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