Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

2405 high risk subjects (1193 patients attending STD clinics, 1012 blood donors and 200 hospital personnel) and 500 apparently healthy individuals representing all the twelve districts of the State of Himachal Pradesh were screened for HBs Ag employing reverse passive haemagglutination (RPHA) technique. HBs Ag positivity was found to be 6.77 per cent in test groups and 3.6 per cent in the control group. Maximum positivity was found in STD patients (9.55 per cent) followed by hospital personnel (8 per cent) and blood donors (3.26 per cent). The highest incidence was noticed in district Kullu and no positive case was found in Lahaul and Spiti district of Himachal Pradesh. Remedial measures for prevention of Hepatitis-B virus infection have been emphasized.
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PMID:Incidence of australia antigen (HBs Ag) in Himachal Pradesh. 209 21

Stored serum samples from the Transfusion-transmitted Viruses Study in the 1970s were tested for the presence of antibody to hepatitis C virus (anti-HCV). Single specimens from five control subjects who did not receive transfusions tested negative for anti-HCV. Of four control subjects who did not receive transfusions and who developed non-A, non-B (NANB) hepatitis after hospitalization, three remained anti-HCV negative; the fourth person with postoperative NANB hepatitis tested anti-HCV positive before the operation. Five transfusion recipients with posttransfusion hepatitis B virus infection remained seronegative; a sixth with NANB hepatitis as well as hepatitis B virus infection had seroconversion for anti-HCV. Five of nine transfusion recipients with NANB hepatitis had anti-HCV seroconversion. These results show that present anti-HCV testing demonstrates an etiologic basis for approximately half of the cases of transfusion-associated NANB hepatitis, particularly those that develop chronicity. Although cases of NANB hepatitis without seroconversion may be explained otherwise, they may be caused by another, presently unidentified, virus.
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PMID:Non-A, non-B hepatitis and antibody to hepatitis C virus. 210 49

Standard methods of virus DNA detection using the polymerase chain reaction can be time consuming and can involve multiple steps in which contamination with exogenous DNA can occur. Therefore, we developed a simplified method for detecting hepatitis B virus DNA in serum. The main advantages of this method are that it can be performed rapidly, consists of only several steps, and has a false positive rate of less than 0.1% in our laboratory. In testing serial samples from five chimpanzees experimentally infected with hepatitis B virus, we found that hepatitis B virus DNA was detected 2-3 weeks before the appearance of hepatitis B surface antigen, and it continued to be detectable 1-3 weeks after the production of antibody to hepatitis B surface antigen. In testing serum from 84 human patients, we found hepatitis B virus DNA in all patients who had hepatitis B surface antigen and hepatitis B e antigen in serum and in 64% of the patients with hepatitis B surface antigen with antibody to hepatitis B e antigen in serum. Also, 3 out of 11 patients who were chronic hepatitis B carriers and who subsequently lost hepatitis B surface antigen were found to test positive for hepatitis B virus in serum. In contrast, all patients who lost hepatitis B surface antigen after acute hepatitis B virus infection or those classified as having non-A, non-B hepatitis tested negative for hepatitis B virus DNA. Thus, the modified PCR technique is a sensitive and rapid method for detecting hepatitis B virus DNA-containing virions in serum.
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PMID:Detection of hepatitis B virus DNA in serum by polymerase chain reaction. Application for clinical diagnosis. 211 44

Controversy exists regarding major histocompatibility complex antigen expression on hepatocytes. In this study, hepatocyte expression of class I and II major histocompatibility complex antigens was investigated in diseased and normal livers, using indirect immunofluorescent staining of mechanically isolated, viable hepatocytes. Hepatocytes were obtained from 76 children: 10 with autoimmune chronic active hepatitis, nine with primary sclerosing cholangitis, nine with chronic hepatitis B virus infection, five after liver transplantation, 19 with extrahepatic biliary atresia, 11 with alpha 1-antitrypsin deficiency, four with idiopathic neonatal hepatitis and nine with histologically normal liver. Immunohistochemistry was performed in all cases; flow cytofluorimetry was performed for class I antigens in 38 cases and performed for class II antigens in 18 cases. From three children with autoimmune chronic active hepatitis and two with chronic hepatitis B virus infection, isolated hepatocytes were also incubated with gamma-interferon before staining and analysis. By fluorescence microscopy, class I antigens were detected on hepatocytes from all children, the highest percentage (100%) of positive cells and the most intense staining were observed in untreated patients with autoimmune chronic active hepatitis or primary sclerosing cholangitis and in those with acute rejection of a liver transplant. Reduced class I antigen expression occurred in chronic hepatitis B virus infection. Class II antigens were only detected on hepatocytes from eight patients: three with autoimmune chronic active hepatitis and five with primary sclerosing cholangitis, all untreated. Flow cytofluorimetric analysis confirmed the results obtained by fluorescence microscopy, but it also demonstrated a weak class II antigen expression during liver allograft rejection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Class I and class II major histocompatibility complex antigen expression on hepatocytes: a study in children with liver disease. 211 17

We have studied antibodies (anti-pol antibody) against the polymerase gene product of hepatitis B virus by solid-phase enzyme immunoassay using synthetic peptides coded for by this gene. Sera from six patients with acute hepatitis B, 112 chronic hepatitis B virus carriers and six healthy individuals with naturally acquired immunity to hepatitis B virus were tested for anti-pol antibody. In acute hepatitis B virus infection, anti-pol antibody was detected in three of six patients. In chronic hepatitis B virus infection, anti-pol antibody was detected in 17 of 29 (59%), in 23 of 33 (70%) of cirrhotic patients and in 18 of 24 (75%) patients with cirrhosis complicated by hepatocellular carcinoma, compared with 4 of 19 (21%) asymptomatic carriers and 2 of 7 (29%) patients with chronic persistent hepatitis. Titers of anti-pol antibody were higher in cirrhotic patients with and without hepatocellular carcinoma than in patients with chronic active hepatitis. The presence of anti-pol antibody, however, had no relationship with hepatitis B virus-associated DNA polymerase activities and other viral replicative markers. As for sera from six healthy individuals with naturally acquired immunity to hepatitis B virus, two (33%) were positive for anti-pol antibody. These results indicate that the immune response toward the polymerase gene product is induced during acute and chronic hepatitis B virus infection. In chronic hepatitis B virus infection, anti-pol antibody may serve as a new marker indicative of a long period of hepatitis B virus-induced hepatitis.
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PMID:Detection of antibodies against the polymerase gene product in hepatitis B virus infection. 239 Oct 62

A prospective surveillance of hepatocellular carcinoma (HCC) using serum alpha-fetoprotein and high-resolution, linear-array, real-time ultrasonography was carried out in 432 patients with clinicopathologically proven chronic type B hepatitis. During a follow-up period of 6-85 mo (median 23, mean 26.9 +/- 16.8 mo), asymptomatic HCC was identified in 8 patients, with a calculated annual incidence of 826/100,000, and 2768/100,000 for patients over age 35 yr. The relative risk of developing HCC in hepatitis B surface antigen-positive chronic hepatitis patients was 2 when compared to those that were hepatitis B surface antigen-negative, and was 5 when compared in patients over age 35 yr. Hepatocellular carcinomas detected by these methods were in a relatively early stage as most tumors were small, only 50% were associated with cirrhosis, 37.5% were positive for hepatitis B e antibody, and most were still resectable. We, therefore, recommend a combination of alpha-fetoprotein and ultrasonography surveillance in patients with chronic hepatitis in order to improve the chance of early HCC detection as well as the chance for successful resection. In addition, the low incidence of cirrhosis and hepatitis B e antibody in these patients with "early" HCCs and the occurrence of hepatitis B e antigen/hepatitis B e antibody seroconversion after HCC had developed suggest that the development of HCC and progression from hepatitis to cirrhosis were two independent (though related) sequelae of chronic hepatitis B virus infection.
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PMID:Early detection of hepatocellular carcinoma in patients with chronic type B hepatitis. A prospective study. 241 25

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 density of HLA Class I antigen on peripheral blood mononuclear cells was evaluated by flow cytometry in the following groups of patients: 41 HBsAg carriers; 12 individuals with chronic non-A, non-B hepatitis, and 4 with acute hepatitis B. Fourteen of the carriers were positive for antibody to human immunodeficiency virus, and all were negative for antibody to delta agent. Elevated levels of Class I antigen were observed in only 19% of patients with chronic hepatitis B virus infection alone. In contrast, 86% of HBsAg carriers with coexistent human immunodeficiency virus infection demonstrated increased expression. These data suggest that HBsAg carriers are capable of sustaining a systemic interferon response to another chronic viral infection and further supports the hypothesis that a defective interferon response exists in chronic hepatitis B virus infection.
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PMID:Elevated HLA class I antigen expression on peripheral blood mononuclear cells of HBsAg carriers with coexistent human immunodeficiency virus infection. 244 45

We measured activities of alpha- and gamma-interferon simultaneously in 198 sera of 70 patients with acute and chronic viral hepatitis using specific and sensitive enzyme immunoassay and immunoradiometric assay. The results were compared with those in patients with influenza and in healthy controls. Twelve out of 28 patients with acute viral hepatitis showed positive alpha-IFN and/or gamma-IFN activities. alpha-IFN was detectable throughout the clinical course while gamma-IFN levels rose in the convalescent phase regardless of etiology. Conversely, in patients with influenza, both alpha-IFN and gamma-IFN levels of initial samples tended to be higher than those of late samples. Six out of 12 patients with chronic active type B hepatitis showed increased alpha-IFN and/or gamma-IFN values during acute deterioration with marked elevation of serum alanine aminotransferase. However, the two interferons did not always appear simultaneously, although either was detectable in both acute and chronic hepatitis. Enhanced alpha-IFN or gamma-IFN activity was not found in asymptomatic chronic hepatitis B carriers or in patients with chronic persistent hepatitis and liver cirrhosis with chronic hepatitis B virus infection, with the exception of 2 cases. Our results indicated that circulating multiple IFN species were present during the clinical course in some patients with acute and chronic viral hepatitis.
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PMID:Serum levels of alpha-interferon and gamma-interferon in patients with acute and chronic viral hepatitis. 249 28

To analyze interleukin-2-dependent immunoregulatory function in hepatitis B virus infection and in other forms of viral hepatitis, levels of soluble interleukin-2 receptors (sIL-2R) were measured by an enzyme-linked assay in sera from patients with acute and chronic viral hepatitis of different etiology. Increased sIL-2R levels were detected in the early phase of acute hepatitis type A and type B, but not during acute non-A, non-B hepatitis. Among 46 patients with chronic hepatitis B virus infection, levels of sIL-2R were significantly increased only in cases with chronic active hepatitis, while they were about normal in chronic persistent hepatitis or in healthy carriers of the infection. These differences were independent of virus replication, being maintained when patients were stratified according to HBeAg/anti-HBe status and to serum HBV-DNA. Nine patients with chronic active hepatitis type B and high sIL-2R levels at presentation were followed prospectively for two to eight years, and in HBeAg-positive patients, the behavior of receptor levels closely paralleled disease activity. These results, which may reflect increased shedding of IL-2R by activated T lymphocytes in patients with active destruction of HBV infected hepatocytes, indicate the usefulness and potential prognostic importance of serum sIL-2R determination in patients with chronic viral hepatitis. Patients with chronic non-A, non-B hepatitis had much lower sIL-2R levels, although their liver disease was similar to hepatitis B cases, suggesting that different pathogenetic mechanisms operate in these patients.
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PMID:Serum levels of soluble interleukin-2 receptors in acute and chronic viral hepatitis. 224 65


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