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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two antigenically distinct subtypes, adw and ayw, of hepatitis B surface antigen (HBs Ag), have been purified from the plasma of anicteric hepatitis patients. Biophysical studies of these purified preparations revealed considerable heterogeneity in their overall surface charge, morphology and molecular weights. Chemical studies revealed that the composition of the particles is complex in that four to six different polypeptides and three glycoproteins were identified. In addition, cholesterol, three polar lipids, and two glycolipids were detected in purified HBs Ag preparations. Antisera, prepared in guinea pigs to individual polypeptides derived from HBs Ag subtypes adw and ayw, reacted with both the group- and type-specific antigenic determinants associated with the intact particles. The potential of these purified preparations of HBs Ag and of the individual subunits derived from them as possible vaccines is discussed. Specific antipolypeptide sera will be utilized to determine whether HBs Ag components are synthesized as specific viral products or are composed of components of modified host-cell molecules.
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PMID:Biophysical and biochemical properties of purified preparations of hepatitis B surface antigen (HBs Ag). 5 5

The principal antigenic determinants of hepatitis-B surface antigen (HBs Ag) are specified by distinct genotypes of hepatitis-B virus (HBV). This hypothesis still stands undisproven. These specificities include the common antigen(s), called a, and two pairs of subdeterminants, d/y and w/r. The members of each pair are in general mutually exclusive, resulting in four "primary" phentoypes of HBs Ag: adw, adr, ayw, and ayr. The newer "a(w) subcategories" probably also reflect differences in viral genotype; if so, the number of "subtypes" rises to eight. Further subdivision into independent strains of HBV may eventually become feasible on the basis of one or more of the following "new" HBs Ag reactivities, once these have been shown to be virus-coded: g, n, q, x, and t. The requirements for accepting new reactivities as HBV-specific, and for comparing them among themselves, are discussed, using t as an example. A peculiar feature of t is its variable physical behaviour: "overt" t reactivity is correlated with the adw phenotype; "cryptic" [t], with ayw; while adr and ayr have so far been t-negative. Pending the indispensable tests of experimental transmission, this uneven distribution would seem to suggest that expression of t is regulated by the HBV genome.
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PMID:Serotypes of hepatitis B antigen (HBs Ag): the problem of "new" determinants, as exemplified by "t". 5 8

Two distinct antigen-antibody systems are associated with the hepatitis B virus (HBV): hepatitis B surface antigen (HBs Ag) and antibody (anti-HBs) and the more recently described hepatitis B core antigen (HBc Ag) and antibody (anti-HBc). Testing of serial serum samples from patients with type B hepatitis demonstrates the regular occurrence of anti-HBc during the course of this disease. In general, highest titers of anti-HBc are seen with prolonged circulation of HBs Ag as in the chronic carrier state. Titers of anti-HBc begin to fall with recovery from HBV infection and anti-HBc appears to be shorter lived than anti-HBs. As such, anti-HBc testing is important in documenting the occurrence of infection with HBV and is of great value in epidemiologic studies and in evaluating the safety and efficacy of hepatitis B immune globulin and HBV vaccines.
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PMID:Antibody to hepatitis B core antigen. 5 10

The frequency distribution of HBs Ag in different parts of the world reveals a relatively high frequency among healthy members of population groups inhabiting areas of high incidence of liver cell carcinoma. Similar high frequencies of HBs Ag are also found in those areas where macronodular cirrhosis is relatively common and is usually complicated by liver cell carcinoma. In geographic areas with low incidence of liver cell carcinoma and macronodular cirrhosis, a relatively low frequency of HBs Ag is usually encountered in the population. The frequency of HBs Ag is relatively higher in patients with liver cell carcinoma with or without cirrhosis than in comparable controls. The subtypes of the antigen do not correlate with the incidence of liver cell carcinoma and there is also no correlation between alpha fetoprotein and HBs Ag in the presence of liver cell carcinoma. HBs Ag is very rarely detected in patients with micronodular cirrhosis or in liver cell carcinoma which may be its complication. It would appear that HBs Ag is necrogenic in the liver and is capable of producing hepatic necroses or hepatitis which may progress to macronodular cirrhosis. The areas of hepatic necroses may either progress to liver cell carcinoma or the resultant macronodular cirrhosis may be complicated by carcinoma. The oncogenic potential of HBs Ag requires further studies.
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PMID:Hepatitis B surface antigen and liver cell carcinoma. 5 11

Progress in research on hepatitis type A has begun to accelerate because of the recent discovery of an antigen associated specifically with hepatitis type A infection and the development of tests for antibody to the antigen. Hepatitis A antigen is associated with 27 nm virus-like particles found in the liver and stool of animals experimentally infected with hepatitis type A and in the stool of humans experimentally or naturally infected with the virus. The density of the particulate antigen when isolated from the liver is 1.34, but antigen particles with densities ranging from 1.32 to 1.40 have been detected in stool. However, antigens from the liver and from the stool appear to be antigenically related. Using immune electron microscopy as a serologic tool for detecting antibody to hepatitis A antigen, we detected antibody in convalescent sera from 100 per cent of patients experimentally or naturally infected with hepatitis type A. In contrast, patients with hepatitis type B or non-B hepatitis not epidemiologically compatible with a diagnosis of hepatitis type A did not have a serologic response to hepatitis A antigen. Antibody was found in approximately 50 per cent of normal individuals tested; the frequency was directly related to age. By the use of immune electron microscopy for the detection of hepatitis A antigen and antibody, the temporal relationship of antigen, antibody and liver damage was determined in experimentally infected humans and chimpanzees. On the basis of serologic comparisons, hepatitis type A does not appear to be related to experimental hepatitis caused by the GB agent of Deinhardt, nor is the hepatitis A antigen serologically related to the fecal antigen of Cross.
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PMID:Relationship of hepatitis A antigen to viral hepatitis. 5 12

The reliable propagation of CR326 strain of human hepatitis A virus in Saguinus mystax marmosets has permitted the development of specific serum neutralization, complement-fixation (CF), and immune adherence (IA) assays for hepatitis A antigen and antibody. The CF and IA assay were made possible by the use of livers of CR326-infected marmosets as a source of hepatitis A antigen. All assays were shown to be specific for hepatitis A. Patients with hepatitis B did not show development of hepatitis A antibody. Hepatitis A antibody appeared following onset of illness, and, in the longest time period studied, has persisted for seven years. Epidemiologic studies have been performed on several Costa Rican families with outbreaks of hepatitis, with the IA and CF assays. Also, several populations in the U.S.A. were studied. These indicated a high incidence of hepatitis A at an early age in Costa Rica and a relatively low incidence of hepatitis A antibody among adults in the U.S.A. It was shown that human immune globulin can be standardized for hepatitis A antibody content by the IA assay. Finally, the IA assay indicated probable hepatitis A antibody in uninoculated chimpanzees, grivet monkeys, and rhesus monkeys.
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PMID:Development and utilization of complement-fixation and immune adherence tests for human hepatitis A virus and antibody. 5 13

Of 108 prospectively followed, multiply transfused, open-heart-surgery patients, 12 (11%) developed hepatitis. Patients received only volunteer donor blood tested for hepatitis-B surface antigen (HBsAg) prior to transfusion by counterelectrophoresis (C.E.P.). 4 of the 12 patients developed hepatitis-B-virus infection. Subsequent testing of donor serums by solid-phase radioimmunoassay (R.I.A.) revealed that an R.I.A.-positive, C.E.P.-negative blood unit was transfused to 3 of the 4 type-B hepatitis cases, but to none of the remaining 104 patients; 3 hepatitis-B cases could probably have been prevented by prescreening of donors by solid-phase R.I.A. 8 hepatitis cases were serologically unrelated to the hepatitis-B virus, the hepatitis-A virus, the cytomegalovirus, or the Epstein-Barr virus. Had R.I.A.-positive donors been excluded, 8 of the 9 residual hepatitis cases (89%) would have represented "non-A, non-B" hepatitis. The existence of previously unrecognised human hepatitis virus(es) is probable.
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PMID:Clinical and serological analysis of transfusion-associated hepatitis. 5 29

Chronic liver disease developing after acute hepatitis type B is well documented, but is not thought to occur after acute hepatitis due to other viruses. However, follow-up of 29 patients in a haemodialysis unit who contracted HBsAg-negative acute hepatitis during 1968-70 revealed 8 cases with raised serum-aminotransferase levels dating from that time. Liver biopsy in 7 of these disclosed chronic aggressive hepatitis in 3, of whom 2 had already progressed to advanced cirrhosis. Chronic persistent hepatitis was present in 2 others, and the remaining 2 had non-specific hepatitis in association with massive iron overload. Immunological studies demonstrated a higher frequency of cellular immunity to HBsAg in those who had previously had acute hepatitis than in those who had not, although the prevalence of humoral antibody was similar in the two groups. One possible explanation for these findings is the presence of immunological cross-reaction at a cellular level between the hepatitis B virus and that responsible for the initial outbreak.
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PMID:Chronic liver disease developing after outbreak of HBsAG-negative hepatitis in haemodialysis unit. 5 71

17 out of 175 cases of early syphilis had clinical, biochemical, and immunological evidence of liver damage. Before penicillin therapy the histological appearance of the liver was abnormal in 14 of the 15 patients from whom biopsy specimens were obtained. In 7 cases, treponemes were seen in the liver. After two months' penicillin therapy the extent and severity of the histological abnormality was reduced. In the repeat liver-biopsy specimens obtained after penicillin treatment no treponemes could be demonstrated. It is suggested that the hepatitis found in these 17 cases of early syphilis was produced by treponemes.
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PMID:Early syphilitic hepatitis. 5 74

A randomised, double-blind, controlled trial has been undertaken to compare the efficacy of hepatitis B immune globulin (H.B.I.G.) with that of immune serum globulin (I.S.G.) for the prophylaxis of viral hepatitis. Participants in the trial were individuals exposed accidentally to material infectious for hepatitis (primarily viral B hepatitis). Preliminary evaluation of the first 302 of the 561 individuals entered into the study indicates that H.B.I.G. significantly reduced the frequencies of both clinical and subclinical hepatitis during the first 3--4 months after the injection. Less than 10% of H.B.I.G. recipients had detectable anti-HBs at the sixth month after the injection, suggesting that H.B.I.G. might need to be given every 3--4 months to continually exposed individuals. Further long-term evaluation is required in order to define more clearly those most likely to benefit from H.B.I.G.
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PMID:Efficacy of hepatitis B immune serum globulin after accidental exposure. Preliminary report of the Veterans Administration Cooperative Study. 5 28


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