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)

The identity of the trans-acting factor encoded by the 1,828-bp BamHI DNA fragment of hepatitis B virus (HBV) that suppresses the transcription of the human beta interferon gene was investigated. Each complete and partial open reading frame (ORF) present within the 1,828-bp BamHI HBV DNA fragment was cloned into a simian virus 40 expression vector, and the resulting gene products were assayed for their ability to inhibit the activity of the regulatory DNA region that governs the expression of the beta interferon gene. Only the proteins encoded by the C ORF inhibited the activity of the beta interferon regulatory DNA region; putative proteins encoded by the partial X, P, and S ORFs present in the 1,828-bp BamHI HBV DNA fragment had no effect. A plasmid encoding only the native HBV core antigen, but not one coding for a truncated core antigen, possessed this inhibitory activity. The inhibition by the core antigen was specific for the regulatory elements of the beta interferon gene; none of a variety of viral transcriptional elements was inhibited.
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PMID:Identification of the hepatitis B virus factor that inhibits expression of the beta interferon gene. 187 Jan 97

Widespread screening of donor blood for hepatitis B led to the recognition that most cases of post-transfusion hepatitis were due to an agent or agents, collectively known as non-A, non-B. Until recently, the causative agent for non-A, non-B hepatitis was unknown. In 1988, a new agent, hepatitis C virus, was identified. It is estimated that 150,000 new cases of hepatitis C occur each year and that one-half of patients with hepatitis C develop chronic liver disease. Hepatitis C is responsible for 15,000 new cases of cirrhosis annually. In 1990, an antibody assay was approved for commercial use. Widespread screening of donor blood with this assay should reduce the risk of transfusion-associated hepatitis C. For those patients already infected, antiviral therapy with alpha interferon may offer the chance of cure or significant palliation.
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PMID:Hepatitis C: prevention and treatment. 190 Nov 88

Interferons represent the rapid defence system against viral infections. This review describes the types of interferon and their effects on chronic viral hepatitis. The role of interferon therapy for hepatitis B has been intensively evaluated over the last few years. Response rates of approximately 30% can be achieved by a 4- to 6-month course of alpha interferon treatment in non-immunosuppressed Caucasian patients. Assessment of interferon therapy for hepatitis C has had to rely on indirect markers of disease activity. Current data available indicate response rates in terms of aminotransferase activities of about 50% of patients treated. However, relapse after discontinuation of alpha interferon treatment is common. At present there is no valid treatment procedure for chronic hepatitis D infection. Only a minority of patients with chronic hepatitis D appears to benefit even transiently from alpha interferon.
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PMID:Interferons in chronic viral hepatitis. 190 16

Liver transplantation in HBs-antigen (HBsAg) positive allograft recipients is associated with a high risk of HBV recurrence some time after surgery. So far, results of measures to prevent recurrent HBV-infection by means of treatment with interferon, hepatitis B vaccination and short-term passive immunization with hepatitis B immunoglobulin (HBIg) or monoclonal antibody to HBsAg (anti-HBs) have been disappointing. In the present study the results of long-term, anti-HBs monitored passive immunization with HBIg is reported. In 23 HBsAg-positive liver transplant recipients an anti-HBs level of greater than or equal to 100 IU/l was maintained for 6 or 12 months, respectively. The rate of recurrent infection was found to be less than 20% under HBIg substitution, whereas 11 graft recipients with no or only short-term HBIg prophylaxis were reinfected by month 15 after transplantation. HBV recurrence was associated with chronic liver disease and recurrent cirrhosis in the allograft.
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PMID:Liver transplantation in HBs antigen (HBsAg) carriers. Prevention of hepatitis B virus (HBV) recurrence by passive immunization. 191 81

Several randomised controlled trials have been undertaken to evaluate the efficacy of alpha-interferon in the therapy of chronic hepatitis B. In patients with HBe antigen-positive disease acquired in adult life the response rates vary from 25-50%. In those infected at birth, response rates are lower. Twenty-one pretreatment variables were assessed for their significance in response prediction using data from 114 patients given alpha-interferon for chronic hepatitis B virus infection. In those patients who had received a minimum of 90 million units per m2 total dose over 12 weeks, a negative anti-human immunodeficiency virus antibody status (p less than 0.001), chronic active hepatitis on liver biopsy (p less than 0.005), high AST level (p less than 0.001), low hepatitis B virus DNA level (p less than 0.001) and a history of acute hepatitis (p less than 0.005) were all associated with an increased likelihood of response on univariate analysis. On stepwise logistic regression analysis, hepatitis B virus DNA, AST and a history of acute hepatitis predicted response independently (p less than 0.05). The most reliable combination of predictive factors was a negative anti-human immunodeficiency virus antibody status, with either a positive history of acute icteric hepatitis and AST greater than 45 IU per liter or no history of acute icteric hepatitis and AST greater than 85 IU per liter, which predicted response in 77% with a specificity of 79% (p less than 0.001). The loss of HBsAg in addition to HBeAg and hepatitis B virus DNA was more likely to occur in patients with chronic infection of less than 2 years duration (p less than 0.001).
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PMID:Treatment of hepatitis B virus infection with interferon. Factors predicting response to interferon. 196 Mar 78

Persistence of HBV replication (serum HBV-DNA and intrahepatic HBcAg) and markers of HBV-induced (IgM anti-HBc positive) liver disease in anti-HBe-positive patients characterize a peculiar form of chronic hepatitis B. This form of hepatitis B prevails in the Mediterranean Basin, Middle and Far East and is associated with the infection of an HBV variant that lacks the capacity to produce HBeAg. We analysed the results of interferon treatment of 90 patients with chronic anti-HBe-positive hepatitis included in four randomized controlled trials. Interferon inhibited viral replication to undetectable levels and ALT normalized in about 70% of patients. However, the effect was transient in the majority of cases and hepatitis B relapsed in 41 to 90% of patients. A discrepancy in the rate of relapses could be explained by a significant difference in patients populations with a higher prevalence of cirrhotic patients in studies with poorer response. Therefore, in advanced anti-HBe-positive chronic hepatitis B, interferon shows a lower efficacy than in HBeAg-positive patients. The earlier treatment starts, the more efficacious is the response to interferon. Future clinical trials should focus on higher doses for longer periods, repeated courses or on combination therapy with nucleoside analogs or immuno-stimulant drugs.
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PMID:Treatment with interferon of chronic hepatitis B associated with antibody to hepatitis B e antigen. 196 Mar 79

In our Pediatric Haemato-Oncology Unit, 42 young patients cured of their malignancy were left with chronic delta hepatitis. The severity of liver disease in many of these patients prompted us to start a pilot study on the effect of recombinant alpha 2b interferon, given at a dose of 5 MU/square meter thrice weekly. All nine patients included in the study (five males, mean age: 15 years) had well-compensated liver disease, including five cases with active hepatitis and cirrhosis. At the end of the 3rd month of therapy, two patients with cirrhosis developed a biochemical exacerbation leading to hepatic decompensation, which was fatal in one case. The reasons for this unfavourable outcome remain unclear. Basic immunological tests were normal, but one of the two patients was the single case with anti-liver-kidney microsome antibodies. On the other hand, both patients seroconverted from hepatitis B e antigen to antibody at the time of exacerbation, suggesting that liver damage could have been the result of cell-mediated cytotoxicity to hepatitis B virus antigens. The results of this study, which has been interrupted at the 4th month, suggest that interferon therapy for chronic delta hepatitis has to be considered cautiously in young patients cured of pediatric malignancies. In fact, no beneficial effect was seen and the treatment appeared to be harmful in at least two out of nine patients treated.
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PMID:Interferon therapy of chronic delta hepatitis in patients cured of pediatric malignancies: possible harmful effect. 196 Oct 87

A 44-year-old man with chronic hepatitis B virus infection and cirrhosis was treated with recombinant human interferon alfa for 67 days immediately before orthotopic liver transplantation and immunoprophylaxis with hyperimmune globulin to hepatitis B virus in the peritransplant period. Dot blots for hepatitis B virus DNA demonstrated marked reduction in viremia after 41 days of interferon alfa treatment. Southern analysis for hepatitis B virus in liver showed a pronounced decrement in actively replicating forms in the explant, although hepatic infection was still detectable. After liver transplantation, tests for serum hepatitis B virus DNA and hepatitis B surface antigen remained negative. The patient died 32 days after transplantation of causes unrelated to hepatitis B virus. DNA isolated from liver and other visceral organs at autopsy showed infection of the engrafted liver and the persistence of monomeric relaxed circular forms of hepatitis B virus DNA in pancreas, kidney, and spleen. Thus, graft reinfection occurred despite aggressive antiviral therapy and immunoprophylaxis combined with liver transplantation. Existing viral serological markers appear insufficiently sensitive to assess residual infectivity.
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PMID:Persistent hepatitis B virus following interferon alfa therapy and liver transplantation. 198 31

Pretrial and posttrial liver biopsy samples from 124 adult patients who participated in two randomized, controlled trials of interferon alfa therapy for chronic hepatitis B virus (HBV) infection were analyzed to determine the effects of interferon on the replication of HBV in the liver. Replicative forms of HBV DNA were detected in the pretrial biopsy samples from all and posttrial biopsy samples from 74% treated patients and 86% controls. Replicative forms of HBV DNA were detected in the posttrial biopsy samples from all patients who remained positive for hepatitis B e antigen and HBV DNA in the serum, in 77% treated patients and 80% controls who cleared HBV DNA in the serum but who remained positive for hepatitis B e antigen, but in only 19% treated patients and 40% controls who cleared HBV DNA as well as hepatitis B e antigen in the serum. Serum alanine aminotransferase levels were significantly lower in patients whose posttrial biopsies did not contain replicative forms of HBV DNA. In summary, we demonstrated that in most patients with chronic HBV infection treated with interferon alfa, serological response was associated with the disappearance of replicative forms of HBV DNA in the liver.
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PMID:Interferon alfa therapy in patients with chronic hepatitis B virus infection. Effects on hepatitis B virus DNA in the liver. 199 97

Fifty-nine patients with prior hepatitis B virus infection underwent orthotopic liver transplantation. During the first 2 mo, mortality was not significantly different in the hepatitis B virus-infected group (25.5%) vs. a hepatitis B virus-immune control group (21%). Beyond 2 mo, the mortality, rate of graft loss, need for retransplantation and incidence of abnormal liver function were significantly higher in the hepatitis B virus-infected group. Treatment of the hepatitis B virus infection was attempted with passive immunization, combined active and passive immunization, alpha-interferon or nothing. The clinical outcome was not significantly influenced by any of these therapies. However, of the patients who lived more than 60 days, 6 of 22 treated with active plus passive immunization were cleared of HBsAg, something achieved once in 16 patients treated with alpha-interferon, never in 3 patients with passive immunization only and once in 4 patients with no therapy. In patients with recurrent hepatitis B virus infection, the pace of hepatitis development in the graft appeared to be accelerated, and this was particularly striking in patients who underwent multiple retransplantations at progressively shorter intervals. None of the patients who became HBsAg-negative had HBeAg preoperatively.
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PMID:Orthotopic liver transplantation for patients with hepatitis B virus-related liver disease. 201 Jan 75


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