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

The ultrastructural study of liver tissues from 38 patients with type B viral hepatitis consistently showed the presence of hepatitis B core antigen of 21-25 nm size in the liver cell nuclei and to a lesser extent in the cytoplasm. This finding and the demonstration of the tubular form of hepatitis B surface antigen in the proliferative degranulated endoplasmic reticulum constituted the etiologic criterion for the diagnosis of the disease. The double-shelled Dane-like particles were frequently found in association with the tubular form of the surface antigen. The core particles were found in the protoplasmic processes of hepatocytes and this correlated with the immunofluorescent microscopic findings that the antigen may be shed into circulation with the protoplasm. The core antigen was found to resist digestion by various enzymes such as protease, DNase, RNase, phospholipase C, lipase, lysozyme, diastase, neuraminidase and hyaluronidase, all of which did not destroy the immunoreactivity as demonstrated by immunoelectron and immunofluorescent microscopy. Similarly, sodium dodecyl sulfate, Tween 80 and mercaptoethanol also had no effect. The formalin-fixed paraffin-embedded liver tissue sections could be treated with protease to facilitate the immunofluorescent staining for the core antigen in tissue.
 ...
PMID:Structural and immunoreactive characteristics of hepatitis B core antigen. 5 6

The sedimentation of radiolabelled 22 nm hepatitis B surface antigen particles was unaffected by treatment with either trypsin or SDS alone, but combined treatment disrupted the particulate nature of the radiolabelled material. Considerable antibody binding activity by the group-specific determinant (a) was preserved after combined SDS and trypsin treatment but was released from the bulk of the radiolabelled protein; gel filtration indicated an approximate mol. wt. of 5000 to 15000 for the released antibody binding material. This material was precipitated by concanavalin A, suggesting the presence of carbohydrate. Its serological activity was remarkably resistant to boiling and to proteolytic digestion, but was partially sensitive to treatment with 0-01 M-periodate or with mixed carbohydrases and neuraminidase, and was greatly reduced by treatment with reducing agent. These data suggest that the stability of the a determinant is due to the structure of the antibody binding site itself, rather than to involvement in the quaternary structure of the particle, and that intact disulphide bonds and carbohydrate, closely related to the antibody binding site, are necessary for the full expression of serological acitivity.
 ...
PMID:Tryptic cleavage of antibody binding sites from hepatitis B surface antigen particles. 6 23

A glycoprotein fraction (fraction VII) suitable for use as a substrate in assays of microbial neuraminidase was prepared from pooled human plasma. It is pasteurised during preparation to eliminate the risk of transmission of serum hepatitis. This results in polymerisation of some of the gamma1-acid glycoprotein, but fraction VII is shown to be an excellent substrate for the neuraminidase of Clostridium welchii (C. perfringens). A sensitive assay procedure is described. A number of factors may interfere with the measurement of NANA released by the action of microbial neuraminidase and procedures are described for evaluation of this problem. Fraction VII is easy to prepare, cheap and available in standard form in large amounts (inquiries should be addressed to J. K. S.); it is recommended for routine use as a convenient substrate for neuraminidase assays.
 ...
PMID:Preparation of a glycoprotein fraction from pooled human plasma and its evaluation as a substrate for the assay of Clostridium welchii (C. perfringens) neuraminidase. 23 36

Using the agglutination of sheep red cells by human antibodies as an indicator of microbial antibody activity, a highly significant association was found between the response to the e antigen of the hepatitis B virus and the formation of strong antibody levels to microbial substances (chi 2(1) = 33). This kind of association was not found among chronic carriers of the hepatitis B virus who do not produce antibodies to the e antigen (chi 2(1) = 3,7). In the presence of e antigen activity, patients with acute virus B hepatitis almost always show significantly reduced levels of antibodies to microbial substances (chi 2(1) = 20). The findings indirectly reveal that e activity is associated with the inability of the liver to trap bacterial antigens. Circumstantial evidence further suggests that the e factor may bear antigens on its immunoglobulin-like structure very similar to microbial cell wall components. Accepting that human antibodies to the T (Thomsen-Friedenreich) antigen represent reactions to cryptantigenic membrane structure of autologous tissues, it was significant to record that increased anti-t activity is always demonstrated when virus B infections progress from the acute to the chronic carrier stage (chi 2(1) = 73). The most intense anti-T activity is commonly found in subjects who produce antibodies to the hepatitis B surface antigen (chi 2(1) = 138). In the presence of e antigen the amount of anti-T in circulation is always significantly depressed. Since this type of depression is not seen in patients with acute virus B hepatitis who lack the e antigen, we suspect that the reduced anti-T levels in e antigen-positive patients are linked with the in vivo exposure of T receptors by microbial neuraminidase.
 ...
PMID:Hepatic infections. Part II. The effect of acute and chronic hepatitis B antigenaemia on the reaction to antibodies to sheep red cells (microbial antigens) and human T-activated cells (exposed autologous tissue antigens). 31 18

The 20 to 25 nm particles of hepatitis B surface antigen were purified from the serum of a carrier chimpanzee. Five major polypeptide species were revealed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis. Treatment of the particles with neuraminidase (EC 3.2.1.18) and galactose oxidase (EC 1.1.3.9) followed by reduction with tritiated sodium borohydride labelled galactose residues in a single glycoprotein with an apparent mol. wt. of 28 000. The glycoprotein was not labelled when neuraminidase treatment was omitted, indicating that the galactose residues are in subterminal positions in the oligosaccharide chains. There was no significant incorporation of radiolabel into lipid. The serological activity of the antigen, as measured by a competitive double-antibody radioimmunoprecipitation assay, was not altered by the labelling procedure nor by exposure to neuraminidase alone.
 ...
PMID:The labelling of galactose residues in hepatitis B surface antigen glycoprotein. 74 7

The expression of selected lymphocyte surface-membrane markers was evaluated in 37 patients with acute viral hepatitis B, 10 of whom were studied serially through the resolving and convalescent phases of disease. Bone marrow-derived (B) lymphocytes were identified by reference to surface immunoglobulin, whereas normal thymus-derived (T) lymphocytes were assayed by their capacity to form spontaneous nonimmune rosettes with sheep erythrocytes (E rosettes, ER). During the acute and resolving phases of viral hepatitis B, the relative and absolute number of ER-positive lymphocytes was significantly reduced, whereas the number of surface immunoglobulin-positive lymphocytes and the absolute lymphocyte count remained normal. This resulted in the appearance of a third population of cells, deficient in respect to both surface immunoglobulin and ER markers. Such cells accounted for nearly 25% of peripheral blood lymphocytes, approximately 5 x 105ml blood. Depression of the number of ER-positive lymphocytes occurred at least once during the course of disease in every patient studied serially, and was observed in 55 of 67 individual assays of the 37 cases of acute viral hepatitis B. Lymphocytes from some patients reacquired ER function when cultured in fetal calf serum but not in the presence of autologous serum. Such autologous serum was capable of suppressing ER function of lymphocytes from normal donors. The extrinsic suppression of er function by a serum factor (designated as the Rosette Inhibitory Factor), was found to be time dependent, characterized by a 4-h latent period and requiring approximately 18 h for maximum attenuation of ER function. The Serum Rosette Inhibitory Factor was: (a) heat and freeze-thaw stable, (b) nondialyzable, (c) physically separable from hepatitis B surface antigen, (d) not a lymphocytotoxic antibody, and (e) had the buoyant density of a lipoprotein. This extrinsic mechanism was observed in 41.8% of patients with reduced numbers of ER-positive lymphocytes. The Rosette Inhibitory Factor was not detectable in the serum of the remaining 58.2% of the cases of acute and resolving viral hepatitis B despite the presence of reduced numbers of ER-positive lymphocytes. The lymphocytes from these cases did not reacquire ER function when cultured in the absence of autologous serum. The mechanisms responsible for the suppression of normal ER function in these cases appears to be intrinsic to the lymphocytes and not the result of a humoral factor. The T lymphocyte lineage of cells deficient in respect to ER function, whether of intrinsic or extrinsic type, was demonstrated by their capacity to form spontaneous rosettes with neuraminidase-treated sheep erythrocytes. Both intrinsic and extrinsic suppression of T lymphocyte ER function commonly occurred during the first 4 wk of acute viral hepatitis B.9 of the 10 patients followed serially continued to manifest defective ER function at 12 wk...
 ...
PMID:Mechanisms responsible for defective human T-lymphocyte sheep erythrocyte rosette function associated with hepatitis B virus infections. 108 96

Hepatitis B surface antigen was adsorbed to insolubilized sialic acid-specific haemagglutinin isolated from the haemolymph of Limulus polyphemus. Treatment of the antigen with Vibrio cholerae neuraminidase (EC 3.2.1.18) resulted in the release of sialic acid and in an increase of the isoelectric point from pH 4-35 (for subtype ad) or 4-9 (for subtype ay) to pH 5-45. Treated, but not untreated, antigen incorporated [14-C]-sialic acid when incubated at 37 degrees C with sialyl transferase (EC 2.4.99.1) and cytidine-5'-monophosphate-[14-C]-sialic acid. The major portion of [14-C]-sialic acid was linked to a glycoprotein with an apparent mol. wt. of 26 x 10-a. De-sialylated antigen had a drastically reduced in vivo life span in rabbit plasma and elicited a higher humoral antibody response than intact antigen (subtype ad). Antigen-stimulated proliferation of lymphocytes, measured 3 months after immunization, was observed only with cells from rabbits injected with neuraminidase-treated antigen.
 ...
PMID:Sialyl residues in hepatitis B antigen: their role in determining the life span of the antigen in serum and in eliciting an immunological response. 114 61

Highly purified woodchuck hepatocyte plasma membranes demonstrated tight specific binding to glutaraldehyde-polymerized serum albumin immobilized on Sepharose macrobeads. This phenomenon was characterized in detail and used for recognition of the plasma membrane constituents involved in binding of the albumin polymer. The hepatocyte membrane-polyalbumin interaction was found to be ligand-specific, saturable, and time-dependent. Other characteristics of a specific receptor-ligand interaction were also noted, including a dependence on the temperature, pH, and ionic strength of the binding medium. Kinetic studies revealed the presence of two classes of binding sites for glutaraldehyde-polymerized albumin on purified membranes. The sites mediating the saturable high-affinity binding of polymer to hepatocyte membranes could not be solubilized by Triton X-100. Binding activity of Triton-insoluble membrane residues was inhibited by heat treatment and proteolysis, and was significantly suppressed by neuroaminidase digestion. These findings suggest a glycoprotein nature for the high-affinity binding sites and indicate that the corresponding receptors apparently are tightly associated with the plasma membrane matrix. In contrast, low-affinity binding of polymeric albumin was inhibited by both Triton X-100 and pronase, was resistant to neuraminidase, and was activated by lipase, suggesting that membrane lipids are important for the binding conduct. In conclusion, these results provide clear evidence that hepatocyte plasma membranes are endowed with at least two classes of chemically distinct binding components, which are able to specifically recognize serum albumin artificially modified by glutaraldehyde treatment. Therefore, they suggest that in vivo hepatocytes may perform a specific receptor-dependent uptake of ligands expressing glutaraldehyde-polymerized albumin specificity. This phenomenon may play an important role in the proposed participation of naturally modified human serum albumin as a bridge in the attachment and penetration into host hepatocyte of hepatitis B virus, which is known to possess a receptor that is specific for glutaraldehyde-cross-linked human serum albumin.
 ...
PMID:Characterization of the binding sites for glutaraldehyde-polymerized albumin on purified woodchuck hepatocyte plasma membranes. 249 21

We describe the coinfection of insects with wild-type and recombinant baculoviruses in which the polyhedrin gene promoter is used to express hepatitis B virus envelope protein (hepatitis B virus surface antigen; HBsAg) or influenza A virus neuraminidase (NA). Viruses were administered per os to larvae of the cabbage looper, Trichoplusia ni, causing an infection that within 5 days resulted in the production of approximately 0.15 mg of HBsAg per insect, representing 1.5% of the total extracted protein, or approximately 2.8 mg of NA per insect, representing 28% of the total extractable protein. The HBsAg and NA produced by infected larvae were purified from insect lysates. These proteins were antigenic as determined by conformation-dependent immunoassays. The NA was enzymatically active with conventional substrates. The method of infection described allows genetic complementation by wild-type virus of recombinant viruses lacking the polyhedrin gene essential for infection per os and has implications for the high-yield production in insect larvae of other recombinant proteins of baculoviruses.
 ...
PMID:Complementation of recombinant baculoviruses by coinfection with wild-type virus facilitates production in insect larvae of antigenic proteins of hepatitis B virus and influenza virus. 264 35

The present studies examined the immunoregulatory factors that modulate T-lymphocyte cytotoxic activity against tumor cells. At 30 days postvaccination with hepatitis B virus surface antigen(s) (HBsAg), peripheral blood lymphocytes (PBL) from HBsAb-seropositive healthy donors showed 8-10-fold increase in their cytotoxic activity against human hepatocellular carcinoma PLC/PRF/5 cells. However, there was no effect against human embryonic liver or lung fibroblasts (WI-35) cells. After cloning, these cytotoxic lymphocytes responded to HBsAg, phytohemagglutinin (PHA), and neuraminidase (VCN) with significant increases in cytotoxicity. These cloned, activated PBL also had no effect on human embryonic liver or lung fibroblasts. Exogenous 5'-triphosphate (ATP) inhibited the lymphocyte cytotoxic activities. The inhibition was ATP concentration-dependent. Also, colchicine, a tubuline depolymerizing agent, inhibited effector cell cytotoxic lymphocyte activity. Colchicine binds to the target cells without causing cell lysis. Preincubation of the cytotoxic lymphocytes with "cold-insoluble globulin" (CIg) protected the cells from ATP and colchicine inhibition.
 ...
PMID:Plasma "cold-insoluble globulin" protects cytotoxic lymphocytes from ATP inhibition: 2. Immunization against viral cell surface antigen stimulates cytotoxic cells to lyse tumor cells. 301 58


1 2 3 Next >>