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)

Using a second generation enzyme immunoassay (ELISA) for the detection of antibodies against Hepatitis C virus (HCV), we investigated the frequency of antibodies anti-HCV and the Alanine Aminotransferase (ALT) plasma levels of 200 patients without history of viral hepatitis, liver diseases, blood transfusions, intravenous drugs abuse, homosexuality, hemodialysis, infection by Human Immunodeficiency Virus (HIV), Hepatitis B virus (HBV), nor workers of health services. There plasma samples (1.5%), were positives for antibodies anti-HCV, all of these samples were confirmed by RIBA (Recombinant Immunoblot Assay). In these three patients, the ALT plasma level were more than two folds the normal upper limit, another six patients had high ALT levels but less than one fold the normal upper limit. None of the infected patients had any clues that suggested the possible way of infection in the clinic history. We concluded that the incidence of Hepatitis C in the studied patients is 1.5% and that the ALT levels could be used to identify Hepatitis C infection.
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PMID:[Anti-HCV in patients without risk factors for hepatitis C. Prospective study in 200 patients]. 750 1

In testing for antibodies to the hepatitis C virus (anti-HCV) in 112 patients with primary hepatocellular carcinoma, 10 of 33 white patients (30%) and 15 of 79 Asian patients (19%) had a positive response to the antibody. The antibody profile to individual hepatitis C viral antigens and the presence of circulating hepatitis C viral RNA were determined in the 25 patients. The anti-HCV antibodies most frequently detected were toward the antigens from the core (C22) and NS3 regions. Serum hepatitis C viral RNA was present in 17 of the 25 patients (68%), and these patients tended to have serum levels of alanine and aspartate aminotransferases higher than those patients without viremia (136 +/- 22 U per liter versus 64 +/- 11 U per liter and 161 +/- 26 U per liter versus 79 +/- 14 U per liter, respectively, both P < .05). Of the 15 Asian patients with hepatocellular carcinoma and anti-HCV, 4 (27%) had coexisting hepatitis B surface antigen (HBsAg) and 13 (87%) had antibodies to either hepatitis B core or surface antigen. Of the 10 white patients with anti-HCV, however, only 1 (10%) had hepatitis B virus antibodies (P < .01). Among 4 Asian patients with coexisting anti-HCV and HBsAg, 1 was found to have serum hepatitis B viral DNA and the other 3 had hepatitis C viral RNA. A history of blood transfusion was obtained from 12 of the 25 patients with anti-HCV (48%); 20 (80%) had coexisting cirrhosis. Our findings support the hypothesis that hepatitis C virus is an important etiologic agent in the development of primary hepatocellular carcinoma in both white and Asian patients in the United States.
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PMID:Evidence for hepatitis C viral infection in patients with primary hepatocellular carcinoma. 751 78

We studied the frequency and time of appearance of antibodies to the hepatitis C virus (HCV) retrospectively in the sera of 127 patients who underwent heart surgery between 1983 and 1986. They received blood from volunteer donors hepatitis B surface antigen (HBsAg) negative with normal serum alanine-aminotransferase levels. A prospective follow-up was carried out every 15 days for at least 6 months from the moment of the transfusion. Of the ten patients who developed biochemical criteria of post-transfusional non-A non-B hepatitis, six seroconverted to anti-HCV (60%). Of the other 117, two were already positive before transfusion (1.51%), one patient showed antibodies only in the first post-transfusional serum (passive transfer), and another two patients with no evidence of post-transfusional hepatitis developed HCV antibodies on the 90th day, remaining indefinitely (afterwards seroconversion without hepatitis); both patients' earlier sera were anti-HCV negative. Four (40%) of the ten patients with post-transfusional hepatitis did not develop any serum markers to known hepatotropic agents. Although these findings do not exclude a viral infection by these viruses, they are consistent with the involvement of an unidentified non-A, non-B, non-C agent.
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PMID:Prevalence of antibodies to hepatitis C virus after blood transfusion in heart surgery. 752 52

Serially collected serum samples from 81 patients with acute non-A, non-B hepatitis were tested for the presence of antibodies to hepatitis C virus (anti-HCV) by a second-generation enzyme immunoassay (EIA) test. Anti-HCV was detected in 56 cases (69%) during the first month, in 61 cases (75%) at 3 months and in 63 cases (78%) at 6 months. In those 18 patients showing anti-HCV negative results in the three determinations, hepatitis C virus (HCV) RNA was tested using a nested polymerase chain reaction (PCR) in the first serum sample and was detected in only one case. Anti-HCV or HCV-RNA positive episodes were considered as acute hepatitis C, while those negative for both markers were classified as acute non-A, non-B, non-C hepatitis. On comparing acute hepatitis C with the non-A, non-B, non-C episodes, no significant differences were found in the presence of jaundice, mean maximum alanine-aminotransferase (ALT) levels and positivity of markers of past hepatitis B virus (HBV) infection. However, patients with hepatitis C were significantly younger than those with non-A, non-B, non-C hepatitis (p = 0.002). Male sex (78.1% vs. 35.3%; p = 0.001), history of parenteral exposure (90.6% vs. 11.8%; p = 0.0001), and progression to chronicity (73.4% vs. 5.9%; p = 0.0001) were significantly more frequent in the HCV-related group. Although other possibilities cannot be excluded, these results suggest that there might be a different infectious agent implicated in the etiology of acute non-A, non-B, non-C hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiological, clinical and biological characteristics of acute non-A, non-B hepatitis with and without hepatitis C virus infection. 752 72

HLA-DR13 has been associated with resistance to two major infectious diseases of humans. To investigate the peptide binding specificity of two HLA-DR13 molecules and the effects of the Gly/Val dimorphism at position 86 of the HLA-DR beta chain on natural peptide ligands, these peptides were acid-eluted from immunoaffinity-purified HLA-DRB1*1301 and -DRB1*1302, molecules that differ only at this position. The eluted peptides were subjected to pool sequencing or individual peptide sequencing by tandem MS or Edman microsequencing. Sequences were obtained for 23 peptides from nine source proteins. Three pool sequences for each allele and the sequences of individual peptides were used to define binding motifs for each allele. Binding specificities varied only at the primary hydrophobic anchor residue, the differences being a preference for the aromatic amino acids Tyr and Phe in DRB1*1302 and a preference for Val in DRB1*1301. Synthetic analogues of the eluted peptides showed allele specificity in their binding to purified HLA-DR, and Ala-substituted peptides were used to identify the primary anchor residues for binding. The failure of some peptides eluted from DRB1*1302 (those that use aromatic amino acids as primary anchors) to bind to DRB1*1301 confirmed the different preferences for peptide anchor residues conferred by the Gly-->Val change at position 86. These data suggest a molecular basis for the differential associations of HLA-DRB1*1301 and DRB1*1302 with resistance to severe malaria and clearance of hepatitis B virus infection.
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PMID:Naturally processed peptides from two disease-resistance-associated HLA-DR13 alleles show related sequence motifs and the effects of the dimorphism at position 86 of the HLA-DR beta chain. 760 34

To study the mechanism of the effects of alpha-interferon (alpha-IFN) on chronic hepatitis B, we examined its effect on hepatitis B virus (HBV)-specific cytotoxic T cells (CTL). Using two different HBV-DNA transfected human myeloma cell lines, one expressing hepatitis B core antigen (HBcAg; C4) and the other expressing hepatitis B surface antigen (HBsAg; S6) as targets in cytotoxic tests in vitro, peripheral blood mononuclear cells obtained from chronic hepatitis B patients who were treated with alpha-IFN were examined for their cytotoxic activity against these transfectants. During the treatment with alpha-IFN, in association with a decline of serum alanine amino transferase levels, CTL activities were significantly reduced. An inhibition study in vitro revealed that alpha-IFN did not directly inhibit these CTL activities, indicating that alpha-IFN may inhibit the induction of CTL, and thereby may be related to the reduction of hepatocyte injury.
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PMID:Effect of alpha-interferon on hepatitis B virus-specific cytotoxic T cells. 762 Jan 3

Disulfide bonds are of crucial importance for the structure and antigenic properties of the hepatitis B virus (HBV) envelope. We have evaluated the role of the eight highly conserved cysteines of the major antigenic region for assembly, secretion, and antigenicity of the envelope proteins. Mutants carrying single or multiple substitutions of alanine for cysteine were analyzed using epitope tagging and transient expression in COS-7 cells. The only single cysteines found to be indispensable for efficient secretion were Cys-107 and Cys-138, but double mutation of Cys-137 and Cys-139 also created a block to secretion. Poorly secreted mutants formed aberrant oligomeric structures. The antigenicity of the secreted or intracellularly retained mutants was analyzed using a panel of six monoclonal antibodies recognizing group- and subtype-specific determinants. We demonstrate that Cys-107 is critical for the structure of the group determinant a, whereas Cys-147, previously implicated in intramolecular disulfide bonding, is dispensable. Mutant proteins lacking Cys-121 and -124, -137, -147, or -149 have grossly distorted structures of the y subtype determinant. Our data raise the possibility that HBV strains carrying cysteine mutations are nonreactive in hepatitis B surface antigen-specific immunoassays.
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PMID:Secretion and antigenicity of hepatitis B virus small envelope proteins lacking cysteines in the major antigenic region. 764 57

The etiology of non-A, non-B hepatitis (NANBH) in renal dialysis patients was determined. Hepatitis C virus was present in many, but its appearance did not correlate with elevated alanine aminotransaminase. When sera from these patients were tested for antibodies against hepatitis B virus (HBV) X antigen and polymerase, 70% were positive. HBV infection was confirmed by polymerase chain reaction using several HBV-specific primer pairs. However, amplification with X region primers failed to yield products in many patients. Cloning and sequencing of these products demonstrated deletions within the X region. Hence, X-deletion variants of HBV are strongly associated with NANBH in renal dialysis patients.
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PMID:X region deletion variants of hepatitis B virus in surface antigen-negative infections and non-A, non-B hepatitis. 765 63

A monoclonal antibody (I-18) was raised against an enneapeptide representing amino acids 125 to 133 of the product of the S gene of hepatitis B virus DNA [S(125-133) segment] with a sequence of Thr-Ile-126-Pro-Ala-Gln-Gly-Thr-Ser-Met. Another monoclonal antibody (T-7) was raised against an S(125-133) segment in which Ile-126 was replaced by Thr-126. In a panel of 16 samples of hepatitis B surface antigen (HBsAg) with known S gene sequences, I-18 reacted with 5 with Ile-126. T-7 reacted with 10 HBsAg samples with Thr-126; it did not, however, react with the remaining one of subtype ayw with Thr-126 flanked by Met-125 and Thr-127. The two allelic subtypic determinants, specified by Ile-126 and Thr-126 and distinct from d/y or w/r, were named i and t after isoleucine and threonine, which regulate them. They were expressed in a mutually exclusive fashion in 216 (83%) of 260 HBsAg samples from asymptomatic carriers. They were not detected in 36 (14%) samples; the failure to detect an i or t determinant was particularly common in HBsAg samples of subtype ayw (26 [79%] of 33). A part of the S gene sequence was determined for eight HBsAg samples without a detectable i or t determinant. They had an Ile-126 or Thr-126 residue that was flanked by Thr-127, not the Pro-127 commonly possessed by HBsAg samples displaying an i or t determinant. Expression of the i/t allele, therefore, would require Pro-127. In eight (3%) of the samples, both i and t determinants were detected; the presence of i and t on the selfsame HBsAg particles was verified by sandwiching the particles between I-18 and T-7. A point mutation from thymine to cytosine at nucleotide 377 in the S gene, contributing different second letters to codon 126 (ATT for Ile and ACT for Thr), would have been responsible for the assembly of HBsAg particles with both i and t determinants by means of phenotypic mixing.
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PMID:Allelic subtypic determinants of hepatitis B surface antigen (i and t) that are distinct from d/y or w/r. 767 9

We have recently developed the technology to identify and characterize the human histocompatibility leukocyte antigen (HLA) class I-restricted, CD8+ cytotoxic T lymphocyte (CTL) response to hepatitis B virus (HBV)-encoded antigens in patients with acute viral hepatitis. CTL are expanded in vitro by stimulation with HBV-derived synthetic peptides and selected by restimulation with a panel of HLA-matched stable transfectants that express the corresponding HBV protein. We have recently reported the existence of an HLA-A2-restricted, CD8+ CTL response to an epitope located between residues 18 and 27 of the HBV nucleocapsid core antigen (HBcAg). We now report the discovery of a CTL epitope located between HBcAg residues 141 and 151 that completely overlaps a critical domain in the viral nucleocapsid protein that is essential for its nuclear localization and genome packaging functions as well as processing of the precore protein. The CTL response to this epitope is dually restricted by the HLA-A31 and HLA-Aw68 alleles, which, unexpectedly, appear to use a common binding motif based on the results of alanine substitution and competition analysis, and the binding properties of these two alleles predicted from their known primary sequence, and from the three-dimensional structure of HLA-Aw68. We have also demonstrated that the HBV-specific CTL response to this epitope is polyclonal during acute viral hepatitis, since these two restriction elements can present the HBcAg 141-151 epitope to independent CTL clones derived from a single patient; and that the CTL response is multispecific, since HLA-A2-restricted and HLA-Aw68-restricted CTL responses to HBcAg 18-27 and HBcAg 141-151, respectively, have been identified to coexist in another patient. The foregoing argue against the emergence of CTL escape mutants as a significant problem during HBV infection, especially at this locus, where mutations might be incompatible with viral replication. Finally, our data suggest an association between the HBV-specific CTL response and viral clearance, and they have implications for the design of immunotherapeutic strategies to terminate HBV infection in chronically infected patients.
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PMID:HLA-A31- and HLA-Aw68-restricted cytotoxic T cell responses to a single hepatitis B virus nucleocapsid epitope during acute viral hepatitis. 767 9


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