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)

Infection by the human immunodeficiency virus is associated with polyclonal B cell activation and increased levels of serum IgA. In order to characterize the molecular species of serum IgA, we have measured total IgA, IgA1, and IgA2 in sera from 60 HIV-1-infected patients and 40 healthy controls. In addition, secretory IgA (S-IgA), secretory IgM (S-IgM), free immunoreactive secretory component (SC), and the distribution of monomeric and polymeric IgA were determined. The data confirm the elevation of total serum IgA levels in HIV-1-infected patients, and both IgA1 and IgA2 concentrations are elevated. Furthermore, the data show a substantial increase in serum levels of both monomeric and polymeric IgA. Serum S-IgA levels were significantly increased in CDC group II patients versus controls and more frequently elevated in CDC group IV patients. The highest S-IgA levels were found among patients with the lowest blood CD4+ cell counts. Serum S-IgA levels were not correlated with serum levels of either total IgA or polymeric IgA. Serum S-IgM levels were also increased in HIV-1-infected patients and positively correlated with serum S-IgA levels. Conversely, serum levels of free SC were not altered. An increase in serum S-IgA was not related to human hepatitis B virus infection and/or to hepatic dysfunction or to diarrhea or overt intestinal infection. The data indicate that secretory Ig (S-IgM and S-IgA), which are likely to be produced at mucosal sites, increase in the serum of HIV-1-infected patients.
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PMID:Secretory immunoglobulins in serum from human immunodeficiency virus (HIV)-infected patients. 135 13

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

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

Sera from 11 patients with fulminant hepatitis B were tested for antibodies to translation products of the pre-S1 and pre-S2 regions of hepatitis B virus of IgM, IgA and IgG classes, as well as of IgA1, IgA2 and SIgA, with solid-phase enzyme immunoassays using native viral polypeptides. Antibodies to pre-S1 region product of IgM and/or IgA class were detected invariably in six patients who still had detectable hepatitis B surface antigen in serum at the time of clinical presentation. The remaining five patients who had lost HBsAg at presentation had antibodies to pre-S region products of various immunoglobulin classes in higher titers. The five patients with fulminant hepatitis without HBsAg had higher levels of IgA antibodies to pre-S region products than the seven patients with nonfulminant acute hepatitis B who had lost HBsAg: IgA antibody to pre-S1 region product (75.6 +/- 63.8 vs. 2.9 +/- 3.2, p less than 0.01) and IgA antibody to pre-S2 region product (28.9 +/- 25.3 vs. 4.2 +/- 6.9, p less than 0.01). IgA antibodies to pre-S1 and pre-S2 region products were invariably polymeric in fulminant hepatitis B. These findings are compatible with the hypothesis that a heightened humoral antibody response to pre-S1 and pre-S2 region products occurs early during the course of fulminant hepatitis B, participating in severe hepatic injury and early clearance of virus characteristic of this disease.
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PMID:Antibodies to translation products of the pre-S1 and pre-S2 regions of the envelope gene of hepatitis B virus in fulminant hepatitis B. 304 36

Solid-phase radioimmunoassays using monoclonal antibodies were used to assay antibody to hepatitis B core antigen of immunoglobulin A class in terms of polymeric and monomeric forms, as well as of IgA1 and IgA2 subclasses, in the serum of persons infected with hepatitis B virus. The level of secretory immunoglobulin A antibody was significantly higher in patients with acute hepatitis (mean +/- S.E., sample per normal ratio = 29.2 +/- 1.9) than that in asymptomatic carriers (2.1 +/- 0.1), patients with chronic persistent hepatitis (3.5 +/- 0.5), patients with chronic active hepatitis (6.9 +/- 1.3) or patients with cirrhosis (5.8 +/- 1.1). In acute type B hepatitis, only polymeric immunoglobulin A antibody of either IgA1 or IgA2 subclass was detected. In contrast, in chronic infection, antibody to hepatitis B core antigen of IgA2 subclass was found in the polymeric form, but antibody of IgA1 subclass was detected in both polymeric and monomeric forms.
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PMID:Immunoglobulin A antibody against hepatitis B core antigen of polymeric and monomeric forms, as well as of IgA1 and IgA2 subclasses, in acute and chronic infection with hepatitis B virus. 373 99

We studied salivary antibodies induced by a seven-valent pneumococcal conjugate vaccine (PncCRM). Healthy Finnish children (n=115), a subcohort of the Finnish Otitis Media (FinOM) Vaccine Trial, were immunised either with the PncCRM or a control vaccine (hepatitis B) at the age of 2, 4, 6, and 12 months. Salivary IgG, IgA, IgA1, IgA2 and sIg for serotypes 6B, 14, 19F, and 23F were measured at 7 and 13 months of age, and IgG and IgA also at 4-5 years of age. The PncCRM could induce both salivary anti-Pnc polysaccharide IgG and IgA. However, by the age of 4-5 years IgA concentrations had increased in both groups and were similar. The increases in IgA concentrations were mostly of IgA1 subclass. The difference between the PncCRM and the control group was more notable for serotypes 6B, 14 and 23F than for serotype 19F. We could not find evidence for the development of mucosal immunologic memory after vaccination with the PncCRM.
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PMID:Salivary antibodies induced by the seven-valent PncCRM conjugate vaccine in the Finnish Otitis Media Vaccine Trial. 1553 Jun 71