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)

The HCV, a single stranded RNA virus belonging to the family of flavivirus, has been identified as the probable cause of the majority of cases of transfusion-associated NANB hepatitis and community-acquired NANB hepatitis in Japan. The hepatitis virus is present in a least 2% of the blood donor population and is extremely common in high risk groups, such as hemophiliacs and hemodialysis patients. The contribution of HCV infection to sporadic, acute and chronic hepatitis, liver cirrhosis and primary liver cancer has been established. Furthermore anti-HCV in 20% of alcoholic patients with liver injury suggest that HCV may be etiologically associated with liver disease previously attributed to other causes. Therapy of acute and chronic liver disease associated with HCV infection is likely to be undertaken with recombinant IFN alpha in the future to prevent the progression of the disease from acute hepatitis to chronic hepatitis, and from chronic hepatitis to liver cirrhosis or primary liver cancer. However the prevention of HCV infection will be the goal, in addition to screening of donor blood and exclusion to a large degree of positive units likely to decrease the incidence of post-transfusion hepatitis.
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PMID:Hepatitis C: basic and clinical studies. 131 82

Interferon-alpha (IFN-alpha) is known to inhibit both DNA and RNA viruses, including hepatitis B virus (HBV). In humans the antiviral effect, if any, of IFN-alpha on hepatitis delta virus (HDV) is complicated by the fact that HDV is spread only to patients already infected with HBV. An in vitro model system was used to assay for an antiviral effect of IFN-alpha on HDV genome replication. Hep G2 cells were transfected with a plasmid containing a trimer of HDV and treated with IFN (20 or 100 units/mL) starting 1-7 days after transfection. RNA extracted from treated and nontreated cells was assayed by both slot blot and Northern analyses. The IFN-alpha treatment as expected increased the 2'-5' oligo A synthetase RNA activity, but it did not affect HDV genome replication. Thus, in the absence of HBV, it appears that HDV is resistant to IFN-alpha.
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PMID:Resistance of hepatitis delta virus replication to interferon-alpha treatment in transfected human cells. 132 4

In 1974, Prince et al. reported the existence of posttransfusion hepatitis with a long incubation period which was not related to hepatitis B virus (HBV). These cases were named "non-A, non-B" (NANB) hepatitis. The genome of NANB hepatitis virus was discovered recently using a recombinant complementary DNA (cDNA) approach. It was termed the hepatitis C virus (HCV), and a specific diagnostic tool for the circulating HCV antibody (anti-HCV) was developed using a purified viral polypeptide derived from recombinant yeast expressing a small part of the HCV genome. HCV is believed to be the main cause of blood-borne non-A, non-B hepatitis worldwide, which frequently evolves to chronic hepatitis and cirrhosis, and which may also be involved in the development of hepatocellular carcinoma. HCV is classified as part of the flaviviridae family and contains a positive-stranded RNA molecule by approximately 10 kb nucleotides. The HCV genome encodes a large polyprotein precursor, which is processed in structural nucleocapsid and envelope proteins and in non-structural proteins (NS1-NS5). Nucleotide sequence comparisons of distinct HCV isolates have shown a significant genetic variability between the different HCV strains. At present the diagnosis of HCV infection depends on various anti-HCV tests including second generation HCV Ab. Antigenic markers for HCV are being developed but the concentrations of HCV antigens in serum are at the lower limit of detectability by existing immunoassay technology. A polymerase chain reaction has been used to detect HCV RNA in the serum and liver. Serum HCV RNA disappears from serum after effective IFN treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fundamental studies of hepatitis C virus: a review]. 133 74

The author presents the new prospects in the treatment of the chronic viral hepatitis in children, which is an up-to-date-problem in the last decade. There are emphasized the present aspects concerning the etiopathogenesis of the disease, which represent a constellation of achievements as a scientific foundation for the therapy: new notions about the viral genome, the mutant viruses, the host's cell-mediated immunity. There are reminded the classifications of the chronic hepatitis and especially the new one of the chronic type B hepatitis, the carries state risks, the vertical transmission from mother to child as an epidemiological source, valid in our country, too. There are specified the findings of the inefficiency and the contraindication of the cortisone and immunosuppressive therapy in patients with proved viral markers (the improvement of the HBV replication and thus, worsening the disease). The present and the future therapy is represented by the antiviral and immunomodulator drugs (alfa-IFN); there are presented the doses, the mode of administration, the predictive and responsivity factors, as well as the combined therapy (prednisone and antivirals). There is concluded that the passive and active immunoprophylaxis in the newborns of HBs Ag-positive mothers in the replicative phase is a great necessity.
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PMID:[An etiopathogenic and therapeutic update in chronic viral hepatitis in children]. 133 70

Intracerebral infection of mice with the neurotropic JHM strain of mouse hepatitis virus usually results in a fatal encephalomyelitis. However, infection with the neutralization resistant mutant, 2.2/7.2-V-2, results in inflammatory cell infiltration of the central nervous system with no apparent clinical symptoms, while conferring resistance to subsequent challenge with a lethal dose of wild type JHMV. The mononuclear cells infiltrating the brains of JHMV variant 2.2/7.2-V-2 infected mice were isolated and characterized. Virus-specific T cells which proliferated in response to JHMV antigen and produced both IL-2 and IFN-g were present among mononuclear cells infiltrating the brain as early as day 5 post-infection. The results suggest that the local immune response within the CNS may be important in dictating the outcome of disease following infections with neurotropic viruses.
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PMID:Virus-specific T cells in the central nervous system following infection with an avirulent neurotropic mouse hepatitis virus. 133 91

Transfection of a plasmid encoding the Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) gene confers resistance to the antiproliferative effect of alpha interferon (IFN-alpha) in EBV-negative U968 cells (P. Aman and A. von Gabain, EMBO J. 9:147-152, 1990). We studied the expression of IFN-stimulated genes (ISGs) in two pairs of Burkitt's lymphoma cell lines, differing in the expression of the putative immortalizing gene of EBV, EBNA2. In EBNA2-expressing cells, the induction of four ISGs by IFN-alpha was strongly reduced or, in some cases, abolished. Chloramphenicol acetyltransferase reporter gene constructs containing different IFN-stimulated response elements were transfected into EBNA2-negative and EBNA2-positive cells. Induction of chloramphenicol acetyltransferase activity by IFN was impaired in EBNA2-positive cells. Also, a reporter gene construct driven by an IFN-gamma-sensitive promoter element was affected. However, as revealed by gel shift assays, EBNA2-positive and EBNA2-negative cells exhibited a nearly identical pattern of IFN-stimulated response element-binding proteins. Most important, activation of the factor ISGF-3, which previously has been shown to be required and sufficient for transcriptional activation of IFN-induced genes, was not inhibited in IFN-resistant cells expressing EBNA2. The mechanism of the EBNA2-related IFN resistance seems to be distinct both from the resistance mediated by hepatitis virus and adenovirus gene products and from the IFN resistance in Daudi cell variants. In these three cases, the transcriptional block of IFN-induced genes is due to inhibition of ISGF-3 activation and binding. Our data suggest that the EBNA2-related IFN resistance in Burkitt's lymphoma cells acts downstream of the activation of ISGF-3.
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PMID:The EBNA2-related resistance towards alpha interferon (IFN-alpha) in Burkitt's lymphoma cells effects induction of IFN-induced genes but not the activation of transcription factor ISGF-3. 140 70

A 28 year old woman with hepatitis B (HB) related chronic active hepatitis was treated with a 12 week course of alpha-interferon (alpha-IFN). She developed acute mono-arthritis 1 week after completion of treatment. Her rheumatoid factor (RF) was positive before alpha-IFN and fell steadily during therapy. This was followed by a rebound of RF level with the associated arthritis occurring 1 week after completion of the course of alpha-IFN. In absence of any medication RF gradually fell and became negative at the end of 1 year. This observation is thought to be related to the immunomodulatory effect of alpha-IFN either directly on RF production or indirectly through the control of hepatitis.
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PMID:Mono-arthritis in a chronic hepatitis B patient after alpha-interferon treatment. 151 71

Thirty-three patients with chronic hepatitis C/non-A, non-B were included in a randomized controlled study of interferon-alpha 2b (IFN-alpha 2b) treatment, 3 x 10(6) U three times weekly for 36 weeks. Using an immunoperoxidase technique, frozen liver biopsy specimens were examined with MoAbs for the presence of T helper cells (CD4), T suppressor/cytotoxic cells (CD8), total T cells (CD2) and B cells (CD22) before and after treatment. beta 2-microglobulin (beta 2-MG) expression on hepatocytes was semiquantified using a scoring system on sections from paraffin-embedded biopsy specimens. Serum levels of beta 2-MG were analysed with a radioimmunoassay technique. Intralobular T helper and T suppressor/cytotoxic cells declined significantly in the treated patients but not in the controls. The portal CD4/CD8 ratio did not change. Before treatment, serum beta 2-MG levels and hepatocyte beta 2-MG expression were significantly higher in patients with chronic active hepatitis compared to patients with chronic persistent hepatitis. Serum beta 2-MG levels increased significantly in responders during IFN treatment, with a maximum after 12 weeks. However, in the liver, the hepatocyte beta 2-MG expression was significantly decreased after treatment. Thus, IFN-alpha treatment does not seem to induce an increased HLA class I antigen hepatocyte expression in chronic non-A, non-B hepatitis, which favours the hypothesis that its anti-viral effects are more important in modulating the disease activity.
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PMID:Lymphocyte subsets and beta 2-microglobulin expression in chronic hepatitis C/non-A, non-B. Effects of interferon-alpha treatment. 154 20

The activity of antibodies to hepatitis C virus (anti-HCV) was investigated in 80 patients with chronic non-A, non-B liver diseases. Anti-HCV antibodies were positive in 82.5% (66/80), and the titers were 1 for 18 patients, 2 for 40 and 3 for 8, respectively. The frequency of anti-HCV was significantly lower in patients with chronic persistent hepatitis (8/13, 61.5%) than in those with chronic active hepatitis (42/49, 85.7%) (P less than 0.05). There was no significant difference in the distribution of anti-HCV titers among the different stages of hepatitis. There was no correlation between anti-HCV titer and histology activity index score in chronic hepatitis. Activity of anti-HCV decreased more frequently in the patients who responded to interferon alpha (IFN alpha) therapy (8/22, 36.4%) than in those who did not (0/9, 0%) (P less than 0.05). These results indicate that anti-HCV activity does not correlate with the activity or disease stage of chronic hepatitis, but that anti-HCV activity decrease more frequently during IFN alpha treatment in patients who responded to IFN alpha therapy.
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PMID:Activity of antibodies to hepatitis C virus of patients with chronic non-A, non-B hepatitis decreases during interferon alpha therapy. 165 65

Nineteen patients with chronic non-A, non-B hepatitis (CH-NANB) and 24 patients with chronic hepatitis B (CH-B) were treated with interferons, and the therapeutic and biological responses of the two groups (CH-NANB and CH-B) were compared. All patients had had sustained elevations in serum glutamic pyruvic transaminase (sGPT) levels for more than 6 months and were proven to have chronic hepatitis by liver biopsy. alpha-Interferon (IFN-alpha) or beta-interferon (IFN-beta) was administered in low doses of 3 to 6 mega international units (MIU) daily for 4 wk. Liver biopsies were taken from 13 CH-NANB and 14 CH-B subjects just before and immediately after treatment, and histological findings were assessed by the histology activity index (HAI) score. SGPT levels decreased much more rapidly and markedly in CH-NANB than in CH-B during IFN therapy (p less than 0.01). The HAI score decreased 3.5 points in CH-NANB and 1.0 point in CH-B between pretreatment and posttreatment. Serum beta 2-microglobulin (beta 2-MG) increased in both types of chronic hepatitis during treatment, but the rate of elevation was significantly less in CH-NANB than in CH-B (p less than 0.001). beta 2-MG expression on hepatocytes stained by the PAP method was almost identical in CH-NANB before and after treatment, whereas it increased steadily in CH-B. The serum 2',5'-oligoadenylate synthetase level increased in both types of hepatitis on IFN administration. These results suggest that, in IFN treatment for CH-NANB, the antiviral actions of IFNs may play a very important role in reducing the activity of chronic hepatitis.
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PMID:Comparative study of clinical, histological, and immunological responses to interferon therapy in type non-A, non-B, and type B chronic hepatitis. 168 84


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