Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A total of 437 patients with hepatitis B were tested for serum HBxAg and anti-HBx in a seroepidemiological study. It was shown that the HBxAg positivity rate was 3.66% (16/437), the anti-HBx positivity rate was 2.97% (13/437). HBxAg was most frequently present in HBsAg, HBeAg, and anti-HBc positive, but anti-HBe negative sera. Anti-HBx was most frequently present in HBeAg and anti-HBc positive, but HBsAg and anti-HBe negative sera. Both the presence of HBxAg and anti-HBx antibodies showed no significant relationship with the presence of serum anti-HBs antibodies. These results indicated that serum HBxAg/anti-HBx system was related to the replications of HBV in the HBV infected human body, and anti-HBx were not protective antibody.
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PMID:[Seroepidemiological study of hepatitis B virus x antigen (HBxAg) and anti-HBx antibodies in patients with hepatitis B]. 130 Dec 63

The hepatitis B virus genome encodes a transcriptional transactivator protein designated HBxAg. We have investigated whether this antigen is a target structure for human T-lymphocytes. Using recombinant HBxAg protein, we found HBxAg-specific stimulation of peripheral blood mononuclear cells in patients with acute hepatitis B virus infection (6 of 6) and chronic hepatitis B virus infection (6 of 17) but not in healthy individuals. With HBxAg-specific synthetic polypeptides, several T-cell epitopes were identified. Most were located in the carboxyterminal half of the HBxAg protein. Five T-cell clones specific for a T-cell epitope located at the carboxyterminal region of HBxAg were established and found to belong to the CD2/CD4-positive, CD8-negative subtype. These data establish for the first time HBxAg as an antigen in the cellular immune response.
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PMID:Immune response of peripheral blood mononuclear cells to HBx-antigen of hepatitis B virus. 170 27

Formalin-fixed, paraffin-embedded specimens from 110 cases of chronic hepatitis and 108 cases of cirrhosis were stained for HBxAg by the avidin-biotin complex technique using specific antisera made against full-length HBxAg polypeptide or derived synthetic peptides. These tissues were also stained for the HBsAg and HBcAg by the peroxidase-anti-peroxidase method. Among patients with chronic hepatitis, 86% were HBsAg positive in liver cells, 60% were surface antigen positive and 32% were core antigen positive. Among patients with cirrhosis, 97% were HBsAg positive in liver cells, 72% were surface antigen positive and 17% were positive for core antigen. Staining specificity was demonstrated, in part, by using preimmune sera in the place of primary antibody, by blocking of the primary antibody with the appropriate antigen before assay and by testing uninfected liver controls. The persistence and high frequency of HBxAg in liver cells from patients with chronic liver disease suggest that it may play one or more important roles in the pathogenesis of chronic infection. It is possible that detection of HBxAg in the liver could be an additional new diagnostic marker for hepatitis B virus infection. However, the function(s) of HBxAg in the pathogenesis of the chronic liver disease, if any, remains to be explained.
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PMID:HBxAg in the liver from carrier patients with chronic hepatitis and cirrhosis. 171 39

Studies were carried out to test the hypothesis that exposure to aflatoxin B1 (AFB1) is common among individuals with hepatocellular carcinoma (HCC) who are also chronically infected with hepatitis B virus (HBV). Experiments were also carried out to determine whether there is a close association between the presence of AFB1-DNA adducts and the expression of one or more HBV antigens in the tumor or non-tumor regions of the liver. Twenty-seven paired tumor and non-tumor liver tissues of HCC patients from Taiwan were analyzed. Monoclonal antibody 6A10, generated against the imidazole ring-opened persistent form of the major N-7 guanine adduct of AFB1, was used for adduct detection by both indirect immunofluorescence and competitive enzyme-linked immunosorbent assay. An avidin-biotin complex staining method was used for the detection of HBsAg and HBxAg in liver sections. A total of 8 (30%) HCC samples and 7 (26%) adjacent non-tumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent non-tumorous liver samples were positive while 9 (33%) HCC samples and 11 (41%) adjacent non-tumor liver samples were HBxAg-positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These results suggest that both AFB1 exposure and carrier status of HBsAg/HBxAg may be involved in the induction of HCC in Taiwan.
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PMID:Aflatoxin B1-DNA adducts and hepatitis B virus antigens in hepatocellular carcinoma and non-tumorous liver tissue. 172 Oct 8

The characteristics of hepatitis B virus (HBV) X antigen (HBxAg) and antibodies against the X antigen (anti-HBx) and the viral polymerase (anti-pol) were determined in 85 HBV-infected patients. HBxAg was detected in sera positive for HBV e antigen (HBeAg) and HBV DNA in patients with acute and chronic hepatitis, while anti-HBx appeared when markers of viral replication became undetectable. HBxAg was common in the liver among patients with chronic hepatitis independent of HBV replication markers but was closely correlated with elevated alanine aminotransferase, implying that HBxAg in liver may be important in the pathogenesis of chronic infection. Anti-pol was detected in many samples positive for HBeAg and HBV DNA and less often in serum samples without markers of HBV replication, suggesting that this marker could reflect ongoing viral replication in the liver, even though such markers were absent from sera.
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PMID:Characteristics of hepatitis B X antigen, antibodies to X antigen, and antibodies to the viral polymerase during hepatitis B virus infection. 195 10

Detection of HBxAg was done by the immunogold-silver staining technique in 22 liver cancer specimens from patients with hepatocellular carcinoma and positive markers of hepatitis B were found to express HBxAg of hepatitis B virus, which was distributed in the perinuclear cytoplasm. The result suggests that HBxAg can be detected practically in all the liver specimens of the patients with hepatocellular carcinoma, who had been infected by hepatitis B virus. The relationship between X gene and its translation product and hepatocellular carcinoma is discussed.
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PMID:[Detection of HBxAg in liver specimens of patients with hepatocellular carcinoma]. 196 3

Human hepatoma cells (HepG2 and HUH7) transfected with a plasmid (pHBV1004) containing the transcription units for the major surface antigen (S) mRNA and the X mRNA of hepatitis B virus (HBV) secreted surface antigen (HBsAg) into the culture medium. A frameshift mutation in the X gene carried by pHBV1004 greatly reduced HBsAg production by cells transfected with an equivalent amount of the mutant (pHBV1004-B). The mutation could be complemented by cotransfection with a plasmid (pSV2HBX) containing the X structural gene under control of the SV40 early promoter. HBsAg production by cells cotransfected with pHBV1004-B and pSV2HBX was equivalent to that in cells transfected with the parent plasmid (pHBV1004) alone. Levels of HBsAg production were directly related to the amount of S mRNA produced, showing that the X-gene product (HBxAg) can modulate expression of the S gene.
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PMID:Modulation of expression of the hepatitis B virus surface antigen gene by the viral X-gene product. 197 36

To clarify the significance of the X gene of hepatitis B virus, we have tested for anti-HBx in the serum and HBxAg in the liver at different stages of the natural history of hepatitis B virus infection. Sera were screened by enzyme-linked immunosorbent assay and positive results confirmed by immunoblot. Purified recombinant MS2 Pol-HBx fusion protein was used as target for both assays. Among serial sera of patients with nonfulminant acute hepatitis, 24 of 64 patients (37.5%) were positive for anti-HBx. In fulminant cases, 15 of 36 patients (42%) had anti-HBx. In chronic hepatitis patients with high rates of hepatitis B virus replication, we found a significantly (p less than 0.01) higher prevalence of anti-HBx, 14 of 25 patients (56%), than in those with low replication, 14 of 66 patients (21%), or among asymptomatic HBsAg carrier blood donors (20 of 126 = 16%) without detectable hepatitis B virus replication (p less than 0.0001). The highest prevalence of anti-HBx was found in HBsAg carriers with cirrhosis (41 of 54 patients = 76%) and/or with hepatocellular carcinoma (18 of 33 patients = 54%). The findings suggest that anti-HBx appears as a common and early marker of hepatitis B virus infection, transient in self-limited hepatitis but persisting with progression to chronicity. In chronic hepatitis, the prevalence of anti-HBx correlated with the intensity and duration of hepatitis B virus replication but neither with the severity of the liver disease nor with malignant transformation per se.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Early and frequent detection of HBxAg and/or anti-HBx in hepatitis B virus infection. 225 44

Immunologically recognizable antigens encoded by hepatitis B virus (HBV) DNA include: (i) the surface antigen (HBsAg), (ii) the pre-S antigen, (iii) the X antigen (HBxAg) and (iv) the core/e antigens (HBcAg/HBeAg). Each one of these antigens or their combination may be prepared for the next generation of vaccines against HBV infection. The synthesis of HBsAg by expression of recombinant DNA in the yeast system has now reached the stage of clinical trials and will certainly provide the first alternative to the currently licensed plasma-derived HBsAg vaccine. The recombinant vaccinia containing the gene encoding HBsAg and transfected cell-lines expressing HBsAg/pre-S gene products are also contenders for alternative vaccines. Synthetic peptide analogues produced by organic synthesis provide experimental immunogens whose potential for the third generation of vaccines appears promising. Among the following group of immunogenic synthetic peptide analogues (PA), PA (139-147) is more promising, because human antibodies in HBsAg-vaccinated individuals predominantly react with this amino acid sequence: HBsAg sequence PA 110-137, 117-137, 125-137, 134-146, 139-147, 138-149. The N-terminal 22 amino acid sequence of the 55 residues preceding the HBsAg sequence, Pre-S (120-145), with the property of binding polymerized albumin. PA HBxAg sequence (100-115, 144-154). PA'HBcAg sequence (73-84).
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PMID:A brief overview of the new vaccines against hepatitis B virus infection: immunogenic gene products and peptide analogues of antigenic epitopes. 242 76

The hepatitis B virus (HBV) genome carries an open reading frame of 462 bases, the X region, but the corresponding protein has yet to be identified as a natural product. In rodent cells cotransformed with the thymidine kinase gene of herpes simplex virus and HBV DNA, however, Gough [1983] identified a mRNA that hybridises uniquely with the X region of the HBV genome. A large fragment of the X region was inserted into plasmid pCL19 delta Y-T in order to produce, in Escherichia coli, the X gene product, HBxAg, as a polypeptide fused to the N-terminal part of the phage lambda cro gene product. Antisera raised against this fused polypeptide gave positive immunofluorescence reactions with the transformed rodent cells. This provides direct evidence for the expression of the HBxAg gene in eukaryotic cells transformed with HBV DNA. The approach used here should be generally applicable.
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PMID:Expression of the X gene of hepatitis B virus. 294 12


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