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)

We previously reported evidence for a statistical association between the serologically determined HLA-Bw54, DR4 and DRw53 alleles and the non-immune responsiveness to hepatitis B virus surface antigen (HBsAg) in the Japanese population. To identify the locus and allele within the HLA region associated with the nonresponsiveness to HBsAg, serological HLA typing, DNA typing of HLA-DQ and DP alleles using amplified HLA genes and sequence-specific oligonucleotide probes, and restriction fragment length polymorphism (RFLP) analysis of the fourth component of complement (C4) genes were performed in healthy unrelated Japanese vaccinees who were immunized subcutaneously three times with plasma-derived HBsAg vaccine. In nonresponders to HBsAg, the frequencies of HLA-Bw54 cross-reactive epitope group (CREG); (Bw54, Bw55, Bw56 and other Bw22), C4 RFLP (6.5 kb + 12.0 kb), DR4, DRw53 and DQw4 (DQA1*0301-DQB1*0401) were increased and the frequencies of HLA-DR1, DRw6 and DQw1 were decreased as compared with those in healthy unrelated controls. Further analysis revealed that the coexistence of HLA-Bw54CREG and DR4-DRw53-DQw4 (DQA1*0301-DQB1*0401) was associated with the nonresponder group, whereas, donors positive for exclusively either Bw54 CREG or DR4-DRw53-DQw4 (DQA1*0301-DQB1*0401) were not associated with the nonresponder group. Because there is a strong linkage disequilibrium between HLA-Bw54CREG, C4 RFLP (6.5 kb + 12.0 kb) and HLA-DR4-DRw53-DQw4 (DQA1*0301-DQB1*0401) in the Japanese population, the extended HLA-Bw54CREG-C4 RFLP (6.5 kb + 12.0 kb)-DR4-DR-w53-DQw4 (DQA1*0301-DQB1*0401) haplotype may well control nonimmune responsiveness to HBsAg. This extended HLA haplotype controls nonresponsiveness as a dominant genetic trait because all ten heterozygotes and two of three probable homozygotes of this extended HLA haplotype were nonresponders.
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PMID:Genetic control of nonresponsiveness to hepatitis B virus vaccine by an extended HLA haplotype. 135 2

In order to investigate the immunogenetic factors associated with hepatitis B virus (HBV) carrier state, the HBe seroconversion and the development of chronic liver disease, HLA typing were performed in 278 asymptomatic HBV carriers (ASC) and 110 patients with chronic B type hepatitis (CH). HLA typing was also performed in 178 vaccinees who had received hepatitis B vaccine. The significantly decreased frequencies of DR1 and DRw13 were found in ASC, CH and non-responders to HB vaccine. This suggests that DR1 and DRw13 may be associated with the elimination of HBV. The frequency of DR4.2 was increased in ASC, but decreased in CH. The seroconversion rate of DR4.2 positive CH as well as ASC was high. Therefore DR4.2 may have relevance to the seroconversion from HBeAg to anti-HBe.
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PMID:[Immunogenetic factors influencing HBV carrier state, the seroconversion and the development of chronic liver disease]. 232 48

The development of antiviral vaccines has been accelerated using monoclonal antibody and/or recombinant DNA techniques, the objective being to prevent grave viral infectious diseases, such as acquired immunodeficiency syndrome (AIDS), adult T-cell leukemia (ATL), and hepatitis B virus (HBV)-associated liver diseases. Certain proportions of individuals in the human population do not have any appreciable immune response to foreign antigens, either in cases of natural exposure or a planned immunization. Here we report that in the nonresponders to HB vaccine, there is an HLA-linked immune suppression gene for hepatitis B surface antigen (Is-HBsAg) controlling the nonresponsiveness to HBsAg through HBsAg-specific suppressor T cells. The Is-HBsAg is in strong linkage disequilibrium with the HLA-Bw54-DR4-DRw53 haplotype.
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PMID:Immune suppression gene on HLA-Bw54-DR4-DRw53 haplotype controls nonresponsiveness in humans to hepatitis B surface antigen via CD8+ suppressor T cells. 296 66

Yeast recombinant hepatitis B vaccine was administered to 25 nonresponders to the plasma-derived hepatitis B vaccine. After three 10-micrograms doses, nine subjects (36%) produced levels of antibodies to hepatitis B surface antigen (anti-HBs) of less than 2.1 sample ratio units (SRU) (nonresponders), and five (20%) developed anti-HBs of 2.1 to 9.9 SRU (hyporesponders); anti-HBs levels of 10 SRU or greater were detected at least once in 11 vaccinees (44%), but by the sixth and 12th months after the last vaccination, only three and one of these "responders," respectively, still maintained anti-HBs values of 10 SRU or greater. In these 25 subjects HLA subtyping showed a high prevalence of DR7, B8, and the combinations of DR3 and DR7 and DR4 and DR7. Our findings indicate that the yeast recombinant hepatitis B vaccine was not effective in eliciting a sustained anti-HBs response in nonresponders to the plasma hepatitis B vaccine.
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PMID:Lack of response to recombinant hepatitis B vaccine in nonresponders to the plasma vaccine. 252 37

504 healthy infants, born to HBsAg negative mothers from May 1st to December 31st 1991, were randomly allocated to an accelerated (group A) or traditional (group B) immunization schedule. The group A infants were immunized at 4 days, 1 month and 3 months of life with 10 micrograms of recombinant HBV vaccine (Engerix B, SKF) while the group B infants were immunized at 4 days, 1 month and 6 months of life with the same dose of vaccine. One month after the first dose of vaccine, 9.2% of the infants in both groups had an HBsAb serum level > 10 mIU/ml. One month after the booster dose, at 4 months of life for group A and at 7 months for group B, 97.40% and 98.53% of the infants presented a serum level > 10 mIU/ml respectively. None in group A and only 2 patients in group B could be considered non-responders (serum concentration below 2 mIU/ml) and 4 infants in group A and 4 in group B were considered hypo-responders (serum level between 2.1 and 9.9 mIU/ml). Immunogenetic study performed on the 2 non-responders and 6 of the hypo-responders, revealed the presence in all but two of the HLA haplotypes, classically involved in the lack of hyporesponsiveness to foreign peptides, namely: HLA-DR7; DQ2, DR4; DQ3, DR15; DQ6 and DR3; DQ2. Surprisingly, 2 hypo-responders carried the HLA haplotypes (DR11, DQ7 and DR13, DQ6), usually associated with hyperresponsiveness. Both vaccinal cycles provided evidence that infants respond well to vaccination, started at birth, against hepatitis B virus with a high degree of protection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Control of hepatitis B: evaluation of two different vaccinal schedules in newborns from HBsAg negative mothers. 836 19

Human leucocyte antigen (HLA)-typing was studied in 82 hepatitis B carriers and 15 cases of autoimmune hepatitis (AIH) to elucidate the genetic factors which may associated with the etio-pathogenesis of chronic hepatitis in Japan. There were two types of HLA phenotypes: HLA A2 was associated with the progression of the disease induced by HBV infection, and HLA A26 and DR5 were related to the retardation of the disease. A family study confirmed the strong association of these HLA phenotypes with the disease induced by HBV infection. In the analysis of AIH, HLA DR4 is a risk factor related to susceptibility of Japanese AIH which shows different clinical manifestations compared to HLA-DR3-positive AIH, dominantly observed in Western countries. These results suggest that genetic background as expressed by HLA, is an important factor in restricting the development of type B hepatitis and AIH, and can explain racial differences of disease susceptibility.
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PMID:Immunogenetic background of hepatitis B virus infection and autoimmune hepatitis in Japan. 848 33

We describe a hepatitis B virus carrier who satisfied the criteria of autoimmune hepatitis proposed by the International Autoimmune Hepatitis Group. A 43-year-old Japanese female showed human leukocyte antigen typing including DR4 in addition to hypergammaglobulinemia, presence of autoantibodies, and liver histology suggestive of autoimmune hepatitis. Moreover, the predominant presence of hepatitis B core antigen in nuclei rather than in cytoplasm of hepatocytes suggested less of a possibility of liver cell damage related to hepatitis B virus infection. She completely responded to immunosuppressive therapy and no clinical or biochemical relapse has been recognized to date.
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PMID:Hepatitis B virus carrier status linked to autoimmune hepatitis. 883 98

Serious adverse effects of immunizations are uncommon. The hepatitis B vaccine has been implicated in a few dozen cases of extraarticular, systemic, or inflammatory joint disorders. We report two cases in which hepatitis A vaccination (Havrix, Smith Kline Beecham) was followed by a connective tissue disorder or a spondylarthropathy in two healthy males aged 50 and 24 years, respectively. Both patients were HLA B27-negative but carried the HLA DR1 and/or DR4 antigen. The outcome was favorable after treatment with a corticosteroid or a nonsteroidal antiinflammatory agent. The pathophysiology of immunization-related rheumatic disorders may involve circulating immune complexes and/or a mechanism similar to that seen in reactive arthritis, i.e., a genetically-determined susceptibility to the bacterial or viral antigens contained in vaccines.
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PMID:Inflammatory joint disease after immunizations. A report of two cases. 980 68

We demonstrated the induction of cell death in a hepatoma cell line by IFN-gamma and its possible mechanism. Among the 2 hepatitis B virus (HBV)-associated hepatoma cell lines, SNU-354 and SNU-368, IFN-gamma induced cell death and increased caspase-3 activity in SNU-368 but not in SNU-354. IFN-gamma induced several changes in the mRNA expression level of apoptosis-regulating genes, e.g., increased expression of Fas, caspase-1 and TNF-related apoptosis-inducing ligand (TRAIL). In particular, IFN-gamma potently increased the mRNA expression of TRAIL in both cell lines. However, it did not change the mRNA expression level of death-mediating TRAIL receptors, e.g., DR4 and DR5, which were constitutively expressed in both cell lines. In contrast, the decoy receptor DcR1 was expressed in SNU-354 but not in SNU-368, and its expression level in SNU-354 was increased by IFN-gamma. Another decoy receptor, DcR2, was constitutively expressed in both cell lines; however, its expression level in SNU-368 was decreased by IFN-gamma. In addition, exogenous recombinant TRAIL reduced viability in SNU-368, but not in SNU-354, cells. From these findings, we speculated that TRAIL up-regulation and the subsequent TRAIL-mediated apoptosis serve as a mechanism of IFN-gamma-induced cell death in SNU-368. To confirm this hypothesis, we demonstrated that soluble DR4-Fc fusion protein, a TRAIL pathway inhibitor, inhibited IFN-gamma-induced cell death in SNU-368. Our results demonstrated that IFN-gamma acts as an inducer of cell death through TRAIL-mediated apoptosis.
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PMID:IFN-gamma induces cell death in human hepatoma cells through a TRAIL/death receptor-mediated apoptotic pathway. 1141 Aug 75