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 incidence of PLC in the Pacific Basin varies from 0.9/100,000 (age-standardized) in women in New South Wales, Australia, to 34.2/100,000 in Singapore Chinese men. Proportional incidence data suggest that other areas of the Pacific Basin, such as Hong Kong, Taiwan, Indonesia, and Papua New Guinea, may have PLC incidence rates as high or higher than those in Singapore Chinese. Infection with hepatitis-B virus has been associated with PLC in some areas, and aflatoxin contamination of food has also been demonstrated. The extent to which these or other factors explain the geographical variation in liver cancer rates in the Pacific Basin is uncertain.
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PMID:Incidence and etiology of primary liver cancer in the Pacific Basin. 53 20

A trimer of hepatitis delta virus (HDV) cDNA in a retrovirus expression vector was transfected into subclone of the PLC/PRF/5 human hepatoma cell line, and a stable cell line (H1 delta 9) was clonally selected that supported the synthesis of both genomic and antigenomic sense HDV RNA. The H1 delta 9 cell line also expressed hepatitis delta antigen (HDAg) in cell nuclei in three distinct morphological patterns, including patterns typically seen in HDV-infected livers. HDAg expression was restricted to the smaller (p24) of the two HDAg-associated polypeptides in early passages of the H1 delta 9 cell line, but continuous passage of the cells resulted in increasing of expression of the larger (p27) HDAg-specific polypeptide. Passage of the H1 delta 9 cells also led to sustained expression of monomeric HDV RNA and a reduction in the levels of dimeric- and trimeric-HDV RNA. This was accompanied by an attenuation of virus-related cytotoxicity which was a feature of early cell passage numbers. HDV RNA replication in these cells was resistant to actinomycin D suggesting that replication was not dependent on continued expression from the transfected HDV cDNA and thus was likely to be self-sustaining.
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PMID:Hepatitis delta virus RNA, protein synthesis and associated cytotoxicity in a stably transfected cell line. 216 31

During the past 15 years, a growing body of evidence incriminates hepatitis B virus as the major factor in the etiology of primary liver cancer. Epidemiological studies throughout the world reported a striking correspondence between areas where the frequency of primary liver cancer is high and where HBV infection is hyperendemic. Moreover, primary liver cancer is commonly associated with cirrhosis of the postnecrotic macronodular type. Such data suggested a sequence hepatitis-cirrhosis-PLC. Such sequence was confirmed by extensive serologic testing studies which reported a high frequency of HBV markers in PLC patients compared to matched control groups. Data collected in Senegal, Mali and Burundi on 12,000 individuals stress the importance of HBV infections in these countries, as the high rate of chronic carrier state in patients suffering from liver cirrhosis or primary liver cancer (62-63%) compared to the general population (12-17%). Other HBV markers including anti-HBs, anti-HBc, HBeAg and anti-HBe had no prognostic value in the sequence hepatitis-cirrhosis-PLC. A new HBV seric marker, the HBsAg/IgM complexes, observed in HBsAg positive individuals, is more frequently detected in PLC patients (50%) and cirrhosis (40%) than in healthy HBsAg carriers (14%). These results would indicate that HBsAg carriers are more likely to develop cirrhosis or primary liver cancer when they evidence HBsAg/IgM complexes. In conclusion, the seric markers of evolution towards primary liver cancer are: HBsAg (the highest known risk factor), the presence in such individuals of HBsAg/IgM complexes, and increased values of alphafoetoprotein.
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PMID:[Hepatitis B and primary cancer of the liver in intertropical Africa]. 241 46

Our study was undertaken to determine whether human recombinant interferon alpha(rIFN alpha), gamma(rIFN gamma), and tumor necrosis factor alpha(rTNF alpha) exert an effect on the HLA-A, B, C expression of human liver cell lines. The HLA-A, B, C expression was assayed by immunoperoxidase staining and enzyme-linked immunosorbent assay. rIFN alpha and gamma enhanced the HLA-A, B, C expression of the three cell lines tested, Chang cells, SK-Hep-1, and PLC/PRF/5. The activity of rIFN gamma proved more than 8000 times more potent than that of rIFN alpha in Chang cells, 30 times in SK-Hep-1, and 20 times in PLC/PRF/5, respectively. rTNF alpha also enhanced the HLA-A, B, C expression of the three cell lines. The enhancement of HLA-A, B, C expression by rIFN alpha and gamma reached a peak on day 3, and that by rTNF alpha on day 5. These findings suggest that IFN alpha, IFN gamma, and TNF alpha may play similar roles in enhancement of HLA-A, B, C expression of hepatocytes in hepatitis and hepatoma cells.
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PMID:Effect of interferon alpha, gamma, and tumor necrosis factor alpha on the HLA-A, B, C expression of cell lines derived from human liver. 249 41

Human primary hepatocellular carcinoma (PLC/342), carried by nude mice, produces hepatitis B core particles as well as hepatitis B surface antigen particles. Core particles purified form PLC/342 tumors displayed epitopes of hepatitis B core antigen (HBcAg) but not epitopes of hepatitis B e antigen (HBeAg) on their surface, unlike core particles prepared from Dane particles, derived from plasma of asymptomatic carriers, that expressed epitopes of both HBcAg and HBeAg. Core particles obtained from PLC/342 tumors were applied to the determination of antibody to HBcAg (anti-HBc) by passive hemagglutination. The assay detected anti-HBc not only in individuals with persistent infection with hepatitis B virus and in those who had recovered from transient infection, but also in patients with acute type B hepatitis, indicating that it can detect anti-HBc of either IgG or IgM class. A liberal availability of core particles from tumors carried by nude mice, taken together with an easy applicability of the method, would make the passive hemagglutination for anti-HBc a valuable tool in clinical and epidemiological studies, especially in places where sophisticated methods are not feasible.
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PMID:Application of hepatitis B core particles produced by human primary hepatocellular carcinoma (PLC/342) propagated in nude mice to the determination of anti-HBc by passive hemagglutination. 300 24

The influence of purified hepatitis B virus surface antigen (HBsAg) preparations or of supernatants derived from PLC/PRF/5 cell line (which produces HBsAg) on human natural killer (NK) activity was examined. Lymphocytes pre-incubated with HBsAg and subsequently washed showed a significant decrease in NK cytotoxicity against K-562 target cells. This effect was reversible and dose-dependent. In addition, pre-incubation with either HBsAg or PLC/PRF/5 supernatants inhibited in a reversible manner lymphocyte--K-562 conjugates and the binding of B73.1 monoclonal antibody (MoAb), which recognizes Fc receptors on NK cells. This effect was not observed with HNK-1, T3, T4, T6, T8 and T11 MoAb. HBsAg was non-toxic to lymphocytes, and ineffective with K-562 target cells. Beta-interferon did not modify HBsAg-mediated inhibition, when added either before or during the contact with HBsAg. Moreover, no modification was observed when neutrophils (at various neutrophil:lymphocyte ratios) were added, even though HBsAg is known to stimulate neutrophils to produce oxygen radicals which may modulate NK activity. We speculate that HBsAg produces these effects by reacting into receptor sites (possibly Fc receptor sites) on NK cell membrane. The overall significance of our results in relation to hepatitis and hepatocellular carcinoma is discussed.
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PMID:Interference of hepatitis B virus surface antigen with natural killer cell function. 404 21

Hepatitis derived from hepatitis B virus (HBV) infection is endemic throughout the world, but it is particularly prevalent in Asia and Africa. In these areas, demographic studies show a strong coincidence between HBV infection (assayed by HBV antigenic markers) and the incidence of primary liver cancer. On these grounds, a causal link between HBV infection and primary hepatocellular cancer has been proposed. Recently, a human hepatoma cell line (PLC/PRF/5; Alexander cells) has been shown to produce hepatitis B surface antigen (HBsAg). We show here that the Alexander cell line contains at least six (four complete and two partial) hepatitis B viral genomes integrated into high molecular weight host DNA. An analysis using specific probes to fragments of the HBV genome suggests that integration of the virus in most cases occurs at the nicked cohesive end region of the virus. Expression of viral sequences using Northern blots demonstrates the presence of RNA transcripts specific for the surface antigen sequences of HBV DNA and the absence of detectable transcripts corresponding to the hepatitis B core antigen.
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PMID:Integration of hepatitis B virus sequences and their expression in a human hepatoma cell. 625 75

Anti-liver-specific membrane lipoprotein (anti-LP-1) and anti-Tamm-Horsfall glycoprotein (anti-THGP) rabbit antibodies were found to bind to Chang liver cells, a cultured human hepatocyte cell line, and PLC/PRF/5, a hepatoma cell line. The antibodies bound were determined by an immunofluorescence staining and a semiquantitative 125I-protein A binding assay. The 125I-protein A binding assay was successfully adapted to determine anti-hepatocyte plasma membrane antibodies in sera of patients with lupoid hepatitis and chronic active hepatitis. The percentage of 125I-protein A bound in 10 normal subjects were 1.5 +/- 0.4 (mean +/- standard deviation) for PLC/PRF/5 and 1.6 +/- 0.6 for Chang liver cell, while those in 2 patients with lupoid hepatitis were 7.2 +/- 0.3, 5.9 +/- 0.1, and those in 8 patients with chronic active hepatitis 3.9 +/- 1.3, 3.2 +/- 1.5, respectively. Furthermore, a blocking study revealed that LP-1 and THGP were partially involved in antigen sites recognized with anti-hepatocyte plasma membrane antibodies in sera of a patient with lupoid hepatitis. The retaining ability of antibody binding to the hepatocytes after the absorption with non-hepatocyte cells suggested the presence of antibodies specific for the hepatocyte plasma membrane in the patient's serum.
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PMID:Hepatocyte plasma membrane antigens. I. Determination of antibodies bound to the hepatocyte plasma membrane by 125I-protein A binding assay. 631 64

Nitrocellulose-protein blotting of serum electrophoresed in agarose gels has been adapted for the study of hepatitis B surface antigen (HBsAg). 125I-labeled anti-HBs was used as the antigen probe, and the electrophoretic migration was monitored by autoradiography. The method required 3 microliter or less of serum and could detect as little as 1 pg of purified HBsAg. Typically, we observed two bands of HbsAg; a moving band which migrated about one-third the distance moved by human serum albumin and a non-migratory band which remained at the loading site. Some examples of the use of the method include: (1) empirical methods for correlating HBsAg concentration in serum to film darkness; (2) observations of mobility changes in serial sera from dialysis patients with chronic HBsAg antigenemia; and (3) detection of related antigens such as antigen from the PLC/PRF/5 hepatoma tissue culture line and the cross-reacting woodchuck patients hepatitis virus surface antigen (WHsAg).
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PMID:The use of nitrocellulose blotting for the study of hepatitis B surface antigen electrophoresed in agarose gels. 702 83

The intrahepatic accumulation of the c-myc protooncogene product was observed on immunofluorescence in each of six patients with chronic hepatitis delta virus infection who exhibited the hepatitis D antigen in their livers. The c-myc product was stained in the same nuclei that contained the hepatitis D antigen. C-myc was not observed in acute hepatitis D or in cases of chronic hepatitis delta virus infection without expression of the hepatitis D antigen. The protooncogene product was detected in only 1 of 32 viral and nonviral liver disorders unrelated to hepatitis delta virus. To confirm these observations, we transfected HBsAg-positive (PCL/PRF/5) and HBsAg-negative (HepG2) transformed liver cell lines with a plasmid containing a hepatitis delta virus cDNA trimer under the control of the SV40 early enhancer/promoter sequences. Whereas baseline c-myc expression was barely detectable in mock-transfected PLC/PRF/5 or HepG2 cells, strong c-myc nuclear fluorescence was observed when these same cells were transfected with the hepatitis D antigen expression vector. Similar results were obtained after infection of HeLa cells with a recombinant vaccinia virus expressing the hepatitis D antigen. Detection of c-myc mRNA sequences by means of in situ hybridization suggested that the c-myc product accumulation was not due to increased amounts of its mRNA. The c-myc protein accumulates selectively in the livers of patients with chronic hepatitis delta virus infection and in the same nuclei that contain the hepatitis D antigen. The expression of c-myc in hepatitis D antigen-containing cells does not require the presence of hepatitis B virus infection.
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PMID:Expression of the c-myc protooncogene product in cells infected with the hepatitis delta virus. 752 69


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