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)

We investigated the effects of interferon therapy on hepatocyte human leukocyte antigen class I and class II antigen expression and intrahepatic lymphocyte subsets in patients with chronic viral hepatitis B (n = 11) and C (n = 10). Interferon-alpha was administered intramuscularly in doses ranging from 3 to 18 million international units daily for 4 wk. Liver biopsy specimens were obtained just before and immediately after treatment, and the specimens were stained by the indirect immunoperoxidase method for evaluation of human leukocyte antigen expression and lymphocyte subsets. Before therapy, no significant difference was noted between hepatitis B and C in human leukocyte antigen class I antigen expression on hepatocytes or in the lymphocyte subsets in the intralobular and portal areas. After interferon-alpha treatment, hepatocyte expression of human leukocyte antigen class I antigens and serum beta 2-microglobulin levels were virtually unchanged in chronic viral hepatitis C patients, but both were increased in chronic viral hepatitis B patients. Human leukocyte antigen class II antigens were not expressed during treatment. The mean number of intralobular CD3+ and CD8+ cells and the mean serum ALT level decreased significantly in chronic viral hepatitis C patients (p less than 0.05) but not in chronic viral hepatitis B patients. The mean number of intralobular CD4+ cells was unaffected by interferon therapy in both groups. In all 21 patients, the changes in CD8+ cell numbers paralleled the changes in serum ALT levels. Our findings suggest that T-cell cytotoxicity may play an important role in hepatocyte damage in both chronic viral hepatitis C and chronic viral hepatitis B and that the response to interferon-alpha differs in these two types of hepatitis.
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PMID:Effects of interferon on intrahepatic human leukocyte antigens and lymphocyte subsets in patients with chronic hepatitis B and C. 171 Oct

Twenty-seven patients suffering from congenital coagulation defects of the prothrombin complex factors were investigated: six had haemophilia B; 14, factor VII defect; four, factor X defect; and three, factor II defect. Nineteen patients (70.3%) had previously received plasma and/or clotting factors concentrates. Among these, markers of hepatitis B infection (HBV) were present in five cases (26.3%) and hepatitis C (HCV) antibodies were found in seven cases (36.8%). The HIV1 prevalence was similarly high. In fact, five patients (26.3%), previously infused with factor IX or prothrombin complex factors concentrates, developed HIV1 infection. No patient with factor VII deficiency became HIV1 positive, despite the administration of unheated factor VII concentrates and the consequent HBV and HCV contamination. In the HIV1 positive group, three patients showed a false positivity for HIV2 antibodies. Five years after seroconversion, three patients developed AIDS (stage IV) and died, one had persistent generalized lymphadenopathy (stage III), and one with post-hepatitis liver cirrhosis was asymptomatic (stage II) for HIV infection. The significant decrease in total white cells, T4 lymphocytes and platelet counts and increase of beta 2-microglobulin and neopterin levels confirmed the prognostic value of these markers for the progression of HIV1 disease. Only one HIV1 negative transfused patient developed anti-HTLV-I p19 antibodies.
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PMID:Prevalence of HIV infection in a cohort of patients with congenital coagulation defects of the prothrombin complex factors. 178 37

Beta 2-Microglobulin expression on hepatocyte membrane was studied in 117 liver biopsies from patients with acute and chronic hepatitis B and in 11 subjects with normal liver function, using immunohistochemical PAP method. In normal liver beta 2-microglobulin could not be detected on hepatocyte membrane, compared with that in subjects with normal liver, in asymptomatic HBsAg carrier and in patients with chronic persistent hepatitis, there is significant enhancement of beta 2-microglobulin expression in patients with acute mild hepatitis and chronic mild active hepatitis. Beta 2-Microglobulin expression in patients with chronic active hepatitis with moderate to severe activity and cirrhosis has a significant enhancement, when compared with acute mild hepatitis and chronic mild active hepatitis. Moreover, location of beta 2-microglobulin expression on hepatocyte membrane was associated with lesion of hepatocytes. Enhanced expression of beta 2-microglobulin on hepatocyte membrane in acute and chronic hepatitis B probably reflects enhanced display of HLA-ABC antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of T cell-mediated hepatocytelysis.
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PMID:[A study of the relation of the expression of beta-microglobulin and hepatocytic lesions in hepatitis B]. 220 29

Recent studies have demonstrated aberrant expression and topographical heterogeneity of HLA Class I and Class II antigens in tissues of patients with certain immunologic or neoplastic diseases. Current information about the expression of HLA antigens by normal and diseased hepatocytes is controversial. We analyzed the HLA antigenic profile of 4 normal fetal livers, 5 normal adult livers, 7 cases of chronic hepatitis B virus (HBV) infection, 14 cases of cirrhosis of various etiologies, 11 hepatic neoplasms, and 5 continuous cell lines derived from hepatic tumors. The specimens were tested by the indirect fluorescent antibody method with a panel of monoclonal antibodies to distinct monomorphic determinants of HLA Class I and Class II antigens and to beta 2-microglobulin. HLA Cells I antigens were not detected on normal fetal and adult hepatocytes, but were displayed on the plasma membrane of hepatocytes in the majority of all hepatic diseases tested and of the 5 hepatic tumor cell lines. There was a significant correlation between the expression of HLA Class I antigens on hepatocytes and the intensity of intralobular inflammation. Double immunofluorescent staining of livers infected with hepatitis B virus demonstrated simultaneous expression of HLA Class I antigens and HBsAg or HBcAg only in a small percentage of hepatocytes, suggesting lack of a specific association between HLA Class I and these viral antigens. HLA Class II antigens were not detected on hepatocytes from any of the liver diseases tested but were expressed by one of the 5 liver carcinoma cell lines analyzed. These findings confirm that HLA Class I antigens are not detectable within the limits of several immunohistochemical methods on normal hepatocytes and suggest that injury by a variety of factors directly or indirectly leads to induction of these antigens on the plasma membrane of hepatocytes.
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PMID:Expression of HLA class I antigens on hepatocytes in liver disease. 242 44

In a chimpanzee model of acute type B hepatitis, at the time of onset of hepatitis B virus replication and before the development of immunity to hepatitis B virus, interferon is present in the plasma. This is followed by an increase in the display of HLA class I, but not class II proteins, on the hepatocyte membrane. In chronic hepatitis B virus infection, there is a low density of HLA class I protein display on the infected hepatocyte. Administration of alpha-interferon enhances HLA display and in many cases is followed by a transaminase elevation, seroconversion of HBe antigen to antibody and disappearance of hepatitis B virus DNA from serum, changes implying clearance of infected hepatocytes. Successful response to interferon therapy may be predicted by a rapidly rising serum beta 2-microglobulin, a component of the HLA class I molecule, during the first 2 weeks of therapy, before the rise in transaminases.
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PMID:HLA class I antigens on the hepatocyte membrane during recovery from acute hepatitis B virus infection and during interferon therapy in chronic hepatitis B virus infection. 242 27

The interferon responsiveness of two cell lines transfected with the hepatitis B virus genome was investigated. A cosmid vector containing multiple copies of the hepatitis B virus genome was transfected into FL5-1 cells; it reduced their sensitivity to interferons as measured by inhibition of the cytopathic effect of Sindbis virus challenge. Similar vectors transfected into HeLa cells reduced their sensitivity to interferon as measured by production of beta 2-microglobulin. This resistance to interferon in hepatitis B virus-transfected cells may be a trans-acting phenomenon related to nucleotide homology between hepatitis B virus DNA and sequences regulating the interferon-induced antiviral system. Alternatively, other mechanisms involving transcription or translation products of hepatitis B virus may be responsible. Hepatitis B virus-induced cellular resistance to the action of interferon may be important in maintaining the chronic carrier state.
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PMID:Defective response to interferons in cells transfected with the hepatitis B virus genome. 246 95

The response rate and HBsAG antibody concentrations were examined after hepatitis B vaccination in 78 hemodialysis patients aged between 29 and 79 years. The values were related to age, duration of hemodialysis, body weight, creatinine, urea nitrogen, serum concentrations of beta 2-microglobulin and soluble interleukin-2 receptor (IL-2R). Patients with low anti-HBsAG antibody concentrations (10-100 mU/ml) had significantly higher IL-2R serum concentrations than those with high anti-HBsAG antibody concentrations (greater than 3,000 mU/ml; p less than 0.05). Discriminant multivariate analysis (p = 0.032) revealed the influence (62%) of IL-2R on the response rate while other factors were similar in all patient groups. It is concluded that preactivation of T cells with an increased release of IL-2R may contribute to impaired immune response after hepatitis B vaccination.
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PMID:Factors influencing the response to hepatitis B vaccination of hemodialysis patients. 252 77

During a randomized controlled trial of interferon and descyclovir therapy, the beta 2-microglobulin and SGOT serum levels in 36 patients with chronic HBe-positive hepatitis B were studied in order to determine whether beta 2-microglobulin has prognostic value for HBe seroconversion. Pretreatment levels of beta 2-microglobulin were elevated in 39% of patients. Significant differences in mean beta 2-microglobulin activity and mean SGOT between treated patients and untreated controls were observed after 4 and 8 weeks of treatment (P less than 0.05). Levels in control patients remained stable. Prior to and during therapy, the mean elevation of beta 2-microglobulin and SGOT levels was similar in responders (N =7) and non-responders (N = 11). The outcome of antiviral therapy in our patients was not dependent on beta 2-microglobulin levels measured before or during interferon therapy.
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PMID:beta 2-Microglobulin and antiviral therapy for chronic hepatitis type B. 266 97

beta 2-Microglobulin display was examined in 131 liver biopsies from patients with acute and chronic type B hepatitis, using an indirect immunoperoxidase method. Enhanced expression of beta 2-microglobulin on hepatocyte membranes was observed in patients with acute hepatitis, chronic active hepatitis with moderate to severe activity and cirrhosis, when compared with normal liver. In acute hepatitis, beta 2-microglobulin-positive hepatocytes were mainly observed in perivenular areas in association with bridging necrosis. In chronic hepatitis, beta 2-microglobulin-positive hepatocytes were observed mainly in periportal zones and in some areas of lobular activity. Diffuse-enhanced display of beta 2-microglobulin on hepatocytes was observed in 5 of 6 patients treated with lymphoblastoid interferon as part of a trial of antiviral therapy. The mechanism by which beta 2-microglobulin display is enhanced on hepatocytes in patients not treated with interferon is uncertain. However, display of beta 2-microglobulin on hepatocytes probably reflects display of HLA-A, B and C antigens and may influence the course of hepatitis B virus infection by increasing susceptibility of the affected cells to T cell-mediated immune attack.
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PMID:Expression of beta 2-microglobulin on hepatocytes in acute and chronic type B hepatitis. 351 Sep 50

We have studied serum and tissue markers of viral replication in 39 patients with chronic hepatitis B virus (HBV) infection and correlated these with periportal and lobular activity in liver biopsies. HBV DNA positivity correlated with the presence of hepatitis B e antigen (HBeAg, P less than 0.001) and aspartate transaminase (AST) levels (P less than 0.005). The lobular but not the periportal inflammatory activity was significantly associated with the presence of HBV DNA (P less than 0.02) and HBeAg (P less than 0.001) and with higher AST levels. The periportal activity correlated with the periportal and lobular display of beta 2-microglobulin on hepatocytes (P less than 0.001 and P less than 0.002, respectively). In patients with chronic HBV infection therefore, the lobular rather than the periportal component of activity was related to viral replication. The association of display of beta 2-microglobulin on hepatocytes with the inflammatory process, in patients with active viral replication, is consistent with the hypothesis that increased display of HLA type I enhances recognition of hepatocytes bearing viral proteins and allows lysis of immune cells.
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PMID:Chronic hepatitis B virus infection. Viral replication and patterns of inflammatory activity: serological, clinical and histological correlations. 354 68


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