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)

Serum immunoglobulin G (IgG) subclasses of hepatitis B core antibody (anti-HBc) in 54 patients with different types of hepatitis B surface antigen positive (HBsAg+) liver diseases (asymptomatic carrier (ASC), acute hepatitis (AH), chronic hepatitis (CH) and liver cirrhosis (LC)) and 18 normal controls were estimated by enzyme-linked immunosorbent assay (ELISA) using subclass specific anti-human mouse monoclonal antibodies. In 11 cases, the estimations were carried out at both exacerbation and remission stages of chronic active hepatitis (CAH). In 4 cases of CAH, serial observations of anti-HBc IgG subclasses were made according to the clinical course. In 5 cases of CAH, the estimations were carried out at the HBe antigen positive (HBeAg+) stage and after sero-conversion to anti-HBe positive (anti-HBe+) stage. In ASC the main anti-HBc IgG subclasses were restricted to one subclass--anti-HBc IgG1. In AH on the other hand, all the subclasses were represented. In CH all the subclasses were detected under different diagnostic conditions but anti-HBc IgG1 was the main subclass. In LC the mean concentration of anti-HBc IgG3 was higher than the concentration of anti-HBc IgG1. In exacerbation stages of CAH, the different anti-HBc IgG subclasses had higher concentrations than in remission stages. The concentrations of different anti-HBc IgG subclasses fell just after seroconversion from HBeAg+ stage to anti-HBe+ stage. These data suggest that the estimation of anti-HBc IgG subclasses may be helpful in establishing the diagnosis of different types and stages of HBsAg+ liver diseases.
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PMID:Immunoglobulin G subclasses of antibodies to hepatitis B core antigen in HBs antigen positive liver diseases. 188 82

The IgG subclasses IgM and IgA1 of antibodies to hepatitis B core antigen (anti-HBc) and hepatitis B e antigen (anti-HBe) were assayed in sera from 82 patients with chronic hepatitis B utilising class/subclass-specific enzyme immunoassays (EIA). The solid-phase was either recombinant hepatitis B core antigen (rHBcAg) or rHBcAg converted to HBeAg by addition of 0.1% SDS with remaining HBcAg antigenicity blocked with monoclonal anti-HBc. Anti-HBc IgG1 was detected in 81 sera at a geometrical mean titre (GMT) of 296,110 x divided by 2.9. Anti-HBc IgG2 was not detected in any of the sera, and anti-HBc IgG3 and IgG4 were detected in 50 and 37 sera, respectively. Anti-HBc IgM and IgA1 were both significantly correlated to the presence of HBV DNA. The predominant antibody to HBeAg was found to be IgG1, being detected in 45 sera with a GMT of 1,035 x divided by 3.3. Anti-HBe IgG2 was not detected in any serum, while anti-HBe IgG3 and IgG4 were found in 8 and 23 sera, respectively. Anti-HBe IgG1, IgG3, and IgG4 were mainly detected in sera positive for anti-HBe in RIA (Abbott). No patient was found positive for anti-HBe IgA1 or IgM. Thus, in contrast to HBcAg, HBeAg does not trigger a persistent IgM and IgA1 response in chronic hepatitis B. The levels of anti-HBe IgG1 and IgG3 were much lower than the levels of anti-HBc IgG1 and IgG3. The presence of anti-HBe IgG4 was significantly correlated to that of anti-HBc IgG4.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of class and subclass distribution of antibodies to the hepatitis B core and B e antigens in chronic hepatitis B. 230 2

The influence of breast and formula feeding on specific anti-hepatitis B surface antigen (HBsAg) IgG subclass production and distribution has been investigated in 40 healthy infants, born to HBsAg-positive mothers and vaccinated against hepatitis B virus (HBV). Twenty children were bottle fed and 20 were breast fed. Specific subclasses were detected at the 4th and 12th months using an enzyme-linked immunosorbent assay with monoclonal antibodies. A defect in total IgG and IgG subclasses was previously excluded. Significant differences were observed both at the 4th and 12th months for IgG1 and IgG2. Breast-fed infants had significantly higher levels of specific IgG2 (about three times higher), while IgG1 levels were significantly higher in formula-fed infants. Anti-HBsAg IgG4 levels were always higher in bottle-fed infants, but a statistical significance was never present. No difference was found in specific IgG3 levels. This study reports the evidence that breast feeding influences specific IgG subclass synthesis against a viral antigen and suggests an immunologic modulation of the response to vaccines dependent not only on age but also on factors present in human milk.
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PMID:Modulation by human milk of IgG subclass response to hepatitis B vaccine in infants. 206 72

The ability to introduce the cloned gene into the mouse germ line has made possible to analyze the cis-acting DNA sequence which is involved in the tissue-specific and developmental regulation of the gene. In addition, this system can also be applied to analyze the patho-physiological roles of the introduced gene product within the mouse whole body. Therefore, this system is one of the best approaches to analyze the mechanism of oncogenesis. The chromosomal translocation is one of the mechanisms leading to the activation of oncogene. In the case of lymphoid cell tumors, the reciprocal translocation between chromosome No. 8 and No. 14 is frequently observed. With this translocation, c-myc gene can be activated by the enhancer of immunoglobulin heavy chain (E mu). We and others have demonstrated that the E mu-myc gene could induce lymphomas in transgenic mice. Following these observation we have currently many examples that activated oncogene can induce variety tumors, giving basic knowledge about the relationship between activated oncogene and cell-type specificity of tumor. On the other hand, molecular mechanism of oncogenesis which is caused by viruses such as hepatitis B virus (HBV) or human T cell leukemia virus (HTLV) is totally unknown. One main reason is the absence of animal model for these diseases. To overcome this problem, we have attempted and succeeded to produce a transgenic mouse model which consistently produces HBV. Using these mice, it will be possible to elucidate the molecular mechanism of development of hepatitis and hepatocellular carcinoma.
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PMID:[Transgenic mice and their use in cancer study]. 249 65

Antibodies to hepatitis B core antigen (anti-HBc) and e antigen (anti-HBe) were assayed in 46 sera from ten patients with acute hepatitis B utilizing immunoglobulin class- and subclass-specific enzyme immunoassays (EIAs). The sera were sampled 1 to 512 days after onset of hepatic symptoms. Four patients cleared HBsAg rapidly, within 24 days, and six patients cleared HBsAg slowly, within 27-74 days after the onset of symptoms. In three of the patients with rapid clearance of HBsAg, hepatitis B virus (HBV) DNA was not detected in sera tested during the first week after onset. The fourth patient was not tested until 12 days after onset and was then found to be negative for HBV DNA. In four of the patients with slow clearance of HBsAg, HBV DNA was present during the first week of illness. In the other two patients, HBV DNA was not detected in the first serum, 11 and 17 days after the onset of illness. Anti-HBc IgM and IgA1 were detected in all patients, with maximum titers shortly after onset. Anti-HBc IgG1 was present in all sera tested. Anti-HBc IgG2 was not detected in any of the sera. Anti-HBc IgG3 and IgG4 were detected in all patient sera, with IgG3 paralleling IgG1, and IgG4 mainly in sera long after onset. Anti-HBe IgG1, IgG3, and IgG4 were detected in three, two, and two patients, respectively. Anti-HBe IgG2, IgM, IgA1, or IgA2 was not found in any patient. The time required for maximum titer of anti-HBc IgG1 was shorter in the patients with rapid clearance of HBsAg.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Immunoglobulin isotypes of anti-HBc and anti-HBe and hepatitis B virus (HBV) DNA elimination in acute hepatitis B. 262 56

An enzyme immunoassay (EIA) for anti-hepatitis B core (HBc) immunoglobulin G1 (IgG1) was compared with a commercial radioimmunoassay (RIA) for anti-HBc antibody (Corab: Abbott Laboratories, North Chicago, Ill.). In parallel tests of 445 consecutive samples, discrepant results were obtained with 2 samples, 1 of which was positive only by the RIA and the other of which was positive only by the EIA for anti-HBc IgG1. In tests of another 192 samples with low blocking activity in the RIA (inhibition range, 90 to 30%), 10 samples gave discrepant results, 5 of which were positive only by the RIA and the other 5 of which were positive only by the EIA for anti-HBc IgG1. Of 12 samples with discrepant results, 11 samples were tested further for anti-HBc IgG3, IgM, and IgA1 by the EIA. Of these, seven samples were positive for anti-HBc IgG1, anti-HBc IgG3, or both. All seven samples were also positive for anti-hepatitis B surface (HBs) antigen. Three samples were negative for anti-HBc IgG1, anti-HBc IgG3, or both but were positive for anti-HBc IgM, anti-HBc IgA1, or both; and one sample was reactive only in the RIA. These four samples were all negative for anti-HBs. Thus, low-level results in the RIA caused by anti-HBc IgM, anti-HBc IgA, or both reflect the unspecific activation of immature B lymphocytes that is not related to previous exposure to hepatitis B virus (HBV). In contrast, the presence of anti-HBc IgG1, anti-HBc IgG3, or both indicates differentiated anti-HBc IgG-producing plasma cells and previous exposure to HBV, as was also shown by the presence of anti-HBs. On class and subclass determination for confirmation of positivity for anti-HBc in 19 serum samples, which was identified by screening of blood from 1,343 donors by a competitive EIA (Hepanostika; Organon), 9 samples with positive results, all low level, did not indicate previous exposure to HBV. It was concluded that determination of classes and subclasses of anti-HBc provides a tool for discriminating positive anti-HBc results not caused by HBV exposure.
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PMID:Enzyme immunoassay for anti-hepatitis B core (HBc) immunoglobulin G1 and significance of low-level results in competitive assays for anti-HBc. 266 17

Nineteen healthy adults were given three injections of hepatitis B vaccine (days 0, 30, and 180), and serum samples were obtained on days 0, 21, 51, and 201. A fourfold or greater increase of IgG antibodies within 201 days was detected in 18 individuals (geometrical mean increase 26-fold), but final IgG antibody concentrations (0.3-3 micrograms/ml) were low. Some vaccines had almost reached peak concentration on day 21, in others a great increase was observed between days 21 and 51, and in a few individuals between days 51 and 201. IgG1 was the predominant subclass in the antibodies of most individuals. Ninety-five per cent of all IgG antibodies were IgG1 in early samples of early responders. In late samples of all vaccinees the average proportion of IgG1 antibodies was 78%. The proportion of IgG2 antibodies was slightly higher in late samples (average 12%) than in the early samples of the early responders, (average less than 6%, P less than 0.05). Considerable amounts of IgG3 and IgG4 antibodies were found in one vaccine, but on the average the proportion of IgG3 or IgG4 antibodies was low (less than 6%).
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PMID:Proportions of IgG subclasses in antibodies formed during vaccination with hepatitis B surface antigen. 294 73

Seventeen adult patients with Down's syndrome (DS) and 19 adult healthy references were vaccinated with a hepatitis B vaccine in order to study the IgG subclass response. An enzyme-linked immunosorbent assay (ELISA) using monoclonal antibodies specific for IgG subclasses was employed. In spite of normal levels of total IgG1 and normal or even high levels of IgG3 in the DS patients, a significantly lower IgG1 response to the vaccine was observed in trisomic patients than in the references.
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PMID:IgG subclass deficiency in patients with Down's syndrome and aberrant hepatitis B vaccine response. 297 59

Human IgG subclasses differ in their biologic functions and are restricted as specific antibodies to certain Ag. The basis for this restriction is unknown but in order to characterize it further, we obtained serum preparations containing one single subclass by using subclass-specific mAb in affinity chromatography. Subsequently we determined the affinity of antibodies in the four IgG subclasses for gp30/p25, a hepatitis B surface Ag (HBsAg) complex, for a nine-amino acid cyclical peptide representing residues 139 to 147 of HBsAg, and for a peptide representing residues 126 to 140 of the hepatitis B virus pre-S2 region and the relative avidity of IgG1 and IgG2 antibodies for purified pneumococcal polysaccharide type 3. Affinities to the HBsAg showed a clear pattern of decreasing affinity in the order IgG1 greater than IgG2 greater than IgG3 greater than IgG4 both in sera from vaccinated and from naturally infected individuals. The relative avidities of antibodies to the polysaccharide Ag had a reverse pattern, IgG2 greater than IgG1. In individuals with or without Ig H chain gene deletions where the anti-HBsAg response was restricted to one subclass, the affinity was similar to that observed for the same subclass in sera from individuals who in addition possessed high or low affinity antibodies of other subclasses.
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PMID:IgG subclass-associated affinity differences of specific antibodies in humans. 313 19

The IgG subclass of antibody associated with hepatitis B surface antigen (HBsAg) in circulating immune complexes (CIC) from patients with either acute or chronic hepatitis B virus (HBV) infections was measured using an isotype and antigen-specific ELISA. All patients were HBsAg positive but were negative for free anti-HBs antibody. The subclass of antibody associated with HBsAg in CIC in both groups was predominantly IgG1 and IgG4. This is in contrast to free anti-HBs in convalescent sera from patients recovering from HBV infection, which are highly restricted to IgG1 and IgG3. The finding of high levels of IgG4 antibodies in CIC suggest that CIC containing this subclass may be cleared less efficiently than CIC containing antibodies of other subclasses. Formation of these CIC may be an important factor in the progression of infection to chronicity and may also be involved in the antigen-specific immunosuppression seen in early acute and chronic HBV infections.
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PMID:IgG subclass composition of antibodies to HBsAg in circulating immune complexes from patients with hepatitis B virus infections. 339 17


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