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)

Rosette inhibitory factor, RIF, previously described in serum from patients with hepatitis B virus infection, has been isolated and identified as a minor species of beta-lipoprotein of the low-density (LDL) class. It is unrelated to hepatitis B virus proteins or particles. Although discrete by reference to charge and density (1.050 +/- 0.004 g/cm3), RIF appears to be a complex macromolecular structure containing apolipoproteins A, B, and C. Greater than 400% recovery is achieved upon 300,000-fold purification from RIF+ sera suggesting activation of a precursor form that is not present in normal serum. RIF inhibits E rosette function of T lymphocytes in vitro with a lag period of approximately 4 h and maximal effect at 24 h consistent with a metabolically-induced event. RIF is functionally active at concentrations of 1 X 10(-12) M or greater, rapidly binds to lymphocytes, and has a functionally effective half-life of approximately 1.5 h. Approximately 2,900 receptors for RIF appear to be present per cell and a high mutual affinity is apparent (k approximately to 9 X 10(10) liters/mol). RIF has no detectable effect on mitogen (PHA) responsiveness of lymphocytes, but inhibits the capacity of lymphocytes to respond to histoincompatible cells in vitro at concentrations greater than 10(-8) M. Equivalent RIF- lipoprotein fractions from normal serum are equally inhibitory in the mixed lymphocyte reaction suggesting that this effect is not directly attributable to RIF activity. These data indicate that RIF is a unique and functionally specific species of LDL that represents either an association complex of lipoproteins or a hybrid molecule of unusual composition. The association of this factor with viral-induced hepatocellular injury underscores the need to elucidate its structure and function in greater detail.
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PMID:Lymphocyte E rosette inhibitory factor: a regulatory serum lipoprotein. 17 85

Lymphocytes from patients with HBs-Ag-positive and -negative acute, chronic-persistent, and chronic-active hepatitis, from healthy controls and from patients with alcoholic liver cirrhosis were tested under standardized conditions. These included use of a single charge of Phytohemagglutinin (PHA-P) dissolved and diluted in one operation, of a single pool of homologous serum of the major blood group AB found free of HBs-Ag and cytotixic factor, and elaboration of PHA dose response curves in the presence of autologous and homologous serum in each case examined. During the early phase of acute virus hepatitis B and non-B, and in HBs-Ag-positive chronic persistent and active hepatitis, hyperresponsiveness of lymphocytes to PHA was observed independently of the source of the serum present in the culture. Lymphocyte responsiveness returned to normal in the later phase of acute hepatitis and depressed in alcoholic liver cirrhosis and in cases of HBs-Ag-positive chronic active hepatitis in which cirrhosis had developed. Although the cause of these alterations in lymphocyte responsiveness is not completely understood, the central role of a primary change of the lymphocytes themselves affecting their ability to react to PHA seems probable.
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PMID:Lymphocyte proliferation to phytohemagglutinin (PHA) in hepatitis B antigen-positive and -negative hepatitis. 44 26

Seventy-two volunteer blood donors who had hepatitis B surface antibody (anti-HBS) were studied and compared with 115 carriers of hepatitis B surface antigen (HBSAg). Anti-BHS-positive donors gave a history of greater possible exposure to hepatitis B virus, there was a lower male-female ratio, and they had a much lower frequency of abnormal hepatic function test results. Those who were positive by counterimmunoelectrophoresis (CIEP), which indicated a high titer of antibody (greater than 1:2,000 as measured by passive hemagglutination assay [PHA], also had an ethnic origin similar to that of the donor panel, ie, predominantly Canadian and northern European. The HBSAg carriers, on the other hand, had a high frequency of origin from Mediterranean and Far Eastern countries. Low-antibody-titer (positive PHA but negative CIEP) donors had ethnic origins that more closely approximated those of HBSAg carriers.
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PMID:Hepatitis B surface antigen and antibody in asymptomatic blood donors. 94 83

Serial studies of PHA-induced lymphocyte transformation, serum autoantibodies, immunoglobulins and complement were performed in seventeen patients with hepatitis A and nine patients with hepatitis B. In both types of hepatitis PHA-induced transformation was markedly impaired during the 1st week after the onset of jaundice and there was less marked but prolonged impairment for a further period of 6-10 weeks. A group of eleven subjects with a previous history of hepatitis had values which were similar to those of healthy persons. Serum from patients with hepatitis A and hepatitis B contains an inhibitor of lymphocyte response to PHA. The inhibitor depresses the function of both patients' and normal lymphocytes and is only detectable during the acute phase of the illness. Washing lymphocytes free from autologous serum did not restore the PHA response to normal but the markedly impaired response present during the first 2 weeks of the illness was improved. A serum factor or factors may therefore be responsible for at least part of the impaired response of lymphocytes to PHA during the acute phase of hepatitis but does not appear to account for the more prolonged impairment of the PHA response. The protracted lymphocyte defect is possibly induced by hepatitis virus. The incidence of autoantibodies and the changes in immunoglobulin levels were similar to those reported by other workers.
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PMID:Immune reactions in acute viral hepatitis. 120 53

Hepatitis B virus (HBV)-associated nucleocapsid antigen (HB core and HB e) is believed to be a major target for T cell-mediated hepatocellular damage in chronic HBV carriers. Studies were undertaken to determine whether both nucleocapsid Ag could be recognized by T cell lines from peripheral blood mononuclear cells (PBMC) from patients with chronic hepatitis B. After cultivation in the presence of rHBcAg or purified HBeAg, growing cells were cloned by limiting dilution in the presence of PHA, IL-2 and allogenic feeder cells. Four HBcAg-reactive and three HBeAg-reactive T cell lines from two patients were generated by proliferation assays. None of the cell lines responded to HB surface Ag or PPD. Four lines were of the CD8+ CD11b- cytotoxic phenotype, two of the CD4+ Leu8- helper phenotype, and the remaining one consisted of mixed populations of CD4+ Leu8+ and CD4+ Leu8- cells. Cross-reactivity study showed that a HBcAg-induced CD4+ T cell line responded to HBeAg, and similarly a HBeAg-induced CD8+ T cell line responded to HBcAg. The reactions were inhibited by HLA class II antibody, but not by class I Ab.
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PMID:T cell lines reactive with hepatitis B core and E antigens in patients with chronic hepatitis B. 166 81

To determine the seroprevalence of hepatitis C virus in the Philippines and compare it with the seroprevalence of hepatitis B virus infection, HBV and HCV markers in 594 serum samples collected from 392 blood donors, 123 medical and paramedical personnel, and 80 patients (45 liver diseases: 25 acute hepatitis, 9 liver cirrhosis, and 11 hepatocellular carcinoma; 28 hepatitis B carriers, and 7 chronic renal failure patients undergoing dialysis) in Davao, Mindanao Island, Philippines, were examined. HBsAg was determined by RPHA, anti-HBc by HI, anti-HBs by PHA, and HBsAg subtypes, HBeAg, and anti-HBe by EIA. HCV markers determined were anti-HCV (anti-C100-3) by ELISA (Ortho Diagnostic Systems), and anti-HCV core (anti-CP9 and/or anti-CP10) also by ELISA. Results showed that 9 (2.2%) blood donors were anti HCV positive; 69 (15.4%) were anti-HCV core positive Nine (2.2%) were HBsAg carriers; 240 (61.3%) were anti-HBs and/or anti-HBc positive (HBsAg carriers excluded from this group). Two of 123 medical and paramedical staff (1.6%) were anti-HCV positive; 11 (8.1%) were anti-HCV core positive; Eight (6.5%) were HBsAg carriers and 81 (65.8%) anti-HBs and/or anti-HBc positive. Five of 11 (45.4%) hepatocellular carcinoma patients were HBsAg carriers; 2 were anti-HCV core positive. Two of 9 liver cirrhosis patients were anti-HCV positive (1 to anti-HCV and the other to anti-HCV core).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Seroepidemiology of hepatitis C virus infection in the Philippines: a preliminary study and comparison with hepatitis B virus infection among blood donors, medical personnel, and patient groups in Davao, Philippines. 190 61

Viral markers of hepatitis B virus (HBV), cytomegalovirus (CMV) and human immunodeficiency virus (HIV), immunoglobulins and complements, T-cell subpopulation antibodies (OKT series) and mitogen responses have been investigated in 68 multitransfused thalassemic patients and in 46 age-matched children. Results showed (1) 56 patients (82.4%) had been exposed to HBV; 29 patients (42.6%) had been exposed to CMV and none were HIV infection. (2) Increased IgG, IgA, OKIal, and decreased C3, OKT3, OKT4, OKT4/OTK8 ratio showed in patients as compared to controls. (3) An apparent increase in lymphocyte proliferation was seen in patients' cultures with or without mitogen (PHA and ConA) stimulation. (4) No definite factors such as sex, age at first transfusion, number of transfusions or HBsAg carrier status correlated with the abnormal change of immunological tests. (5) Immunological investigation, done on 2 occasions six months apart, revealed no significant modifications except that 13 patients (19%) who were initially seronegative for CMV converted to seropositive. These investigations suggest that, although saline-washed RBC was used for the transfused patients, there was high prevalence of HBV and CMV infection. Further studies of lymphocyte function (i.e. lymphokines) are needed to understand the increased spontaneous proliferation in culture and PHA, ConA mitogen responses.
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PMID:Immunologic and virologic status of multitransfused thalassemic patients. 216 12

Studies were undertaken to evaluate the effect of hepatitis B virus (HBV) immune complexes (HBV-IC) on IL-2 dependent human lymphocyte proliferation. The following parameters were studied: 1) Effect of HBV-IC (HBsAg-IgG or HBeAg-IgG) on PHA-mediated lymphocyte proliferation; 2) Influence of HBV-IC on the ability of PHA-stimulated peripheral blood lymphocytes (PBL) for IL-2 production and IL-2 receptor expression. HBV-IC induced a dose dependent and antigenic dependent suppression of PHA stimulated lymphocytes. The suppressor effect exerted by HBsAg-IgG was irreversible. In contrast, the suppression mediated by HBeAg-IgG was reversible: lymphocytes preincubated with this preparation washed and activated with PHA responded well to mitogen. The presence of HBV-IC in the cultures of PHA-activated PBL decreased their ability to produce IL-2: HBeAg-IgG exerted a stronger suppressor effect. This effect was partially reversible: removal of HBV-IC from the culture by washing and subsequent stimulation of PBL with PHA increased the capacity of lymphocytes to produce IL-2. This was particularly evident with HBeAg-IgG. Decreased activity of IL-2 observed in the cultures, was also partially dependent on the ability of HBV-IC to bind IL-2 present in the culture medium. Experiments performed using ultracentrifugation indicated that HBV-IC, especially HBsAg-IgG, may bind to IL-2 and inactivate it. HBV-IC had also an effect on IL-2 receptor expression: 1) their presence in the cultures of PHA-stimulated PBL decreased the number of Tac positive cells; 2) the response of HTCL to exogenous IL-2 was decreased by HBV-IC present in the culture medium. This was especially observed in the case of HBsAg-IgG. We suggest that the observed inhibition of PHA-induced lymphocyte proliferation exerted by immune complexes containing HBsAg-IgG or HBeAg-IgG may be caused mainly by their influence on IL-2 dependent mechanism of lymphoproliferation.
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PMID:Influence of immune complexes containing HBsAg and HBeAg on IL-2 dependent human lymphocyte proliferation. 234 99

Fourteen hybridoma clones have been isolated producing the monoclonal antibodies to the surface antigen of the hepatitis B virus (HBsAg). Monoclonal antibodies have been shown to react in high titres with HBsAg in the reactions of PHA, PH and ELISA. The specificity of monoclonal antibodies to two antigenic determinants has been found by the competitive solid phase ELISA technique. Monoclonal antibodies from nine clones react with one determinant while monoclonal antibodies from the rest five clones react with the other nonoverlapping determinant.
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PMID:[Properties of monoclonal antibodies interacting with determinants of hepatitis B virus surface antigen]. 243 78

Hepatitis B core (HBc)Ag-specific T cells present in the peripheral blood of a patient with chronic active hepatitis B were expanded by co-cultivation for 7 days with rHBcAg. After cloning at 1 cell/well in the presence of PHA and IL-2, five HBcAg-specific CD4+ cloned lines were obtained. All five lines proliferated and produced IL-2, IFN-gamma, and TNF in a dose-dependent fashion in response to HBcAg, but not to HBV envelope Ag. The cloned lines and derivative clones were HLA class II (DR1) restricted. All T cell clones were able to induce anti-HBc production by autologous B cells in response to HBcAg (helper effect). The proliferative response and the helper effect of the HBcAg-specific T cell lines and clones were augmented by co-cultivation with an autologous, autoreactive (HLA-DQ1 specific) T cell clone, even in the absence of HBcAg, and the autoreactive T cells directly stimulated anti-HBc secretion by autologous B cells, presumably due to the release of Ag-nonspecific factors. These findings define a model immunoregulatory circuit the physiologic significance of which remains to be determined.
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PMID:Functional modulation of hepatitis B core antigen-specific T lymphocytes by an autoreactive T cell clone. 245 43


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