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)

Previous work has shown that the hepatitis B x antigen (HBxAg) and antibodies directed against the polymerase of hepatitis B virus (anti-pol) are early markers of hepatitis B virus (HBV) replication in natural infections. The present study was carried out to test the hypothesis that the appearance of one or both of these markers signaled reactivation in chronic carriers with liver disease who were treated with alpha-interferon (IFN). The results show that HBV DNA decreased among the patients who responded to therapy, and that among these responders, neither HBxAg nor anti-pol became detectable in serum for 12 months after treatment, in contrast to controls. Hence, the loss of HBxAg and anti-pol correlate with decreased levels of HBV DNA in response to IFN therapy. However, different patterns of HBxAg and anti-pol were observed among alpha-IFN-treated HBV carrier patients who were also chronically infected with the hepatitis delta virus (HDV). The treatment of such patients often resulted in the loss of HDV RNA from serum and delta antigen from liver. Most of these patients had increased levels of HBV DNA in serum. HBxAg and/or anti-pol also became detectable in patients who lost markers of HDV, implying that the suppression of HDV by IFN is accompanied by the appearance of early markers of HBV reactivation in some of the treated patients.
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PMID:Hepatitis B x antigen and polymerase antibodies in the serum of hepatitis B carriers with or without hepatitis delta virus infection. Effects of interferon treatment. 150 Jun 93

Five viruses are responsible for the vast majority of cases of viral related hepatitis. They have been named hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), hepatitis E virus (HEV). The more recent literature concerning the viral structure, the epidemiology, the serological identification, the clinical course and the prevention of each type of hepatitis is reviewed. HBV is not directly cytopathic. Hepatitis is a consequence of the destruction of the virus-infected cells. The efficient elimination of the virus relies on the viral antigenic determinants (HBs, pre-S1, pre-S2, HBc, HBe) and on the immune system of the host. The viral persistence may be caused by defect of the host immunity (interferon production, T and B lymphocyte function) or by factors related to the virus such as a genome mutation (lack of HBe formation). Some evidence suggesting an immunopathogenetic mechanism also for HCV, HDV and HAV is reported.
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PMID:Nosography and immunopathogenesis of viral hepatitis. 150 25

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

Maternal-infant transmission of hepatitis B virus (HBV) infection is estimated to account for 40-50% of HBV carriers in Chinese populations, but is uncommon among other ethnic groups. The high frequency of maternal-infant transmission among Chinese populations is related to the high prevalence of carrier mothers with replicative HBV infection. The natural course of perinatally acquired HBV infection consists of three phases: an initial phase of immune tolerance followed by a phase of immune clearance and then a non-replicative phase. The initial phase of immune tolerance which may last for several decades contributes to the poor response to interferon therapy. The high prevalence of carrier mothers with replicative infection mandates a combination of passive and active prophylaxis for the newborns.
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PMID:Natural history and control of perinatally acquired hepatitis B virus infection. 155 Dec 46

Ongoing hepatitis B virus replication in the presence of antibody to HBeAg can be observed in patients with active liver disease. These forms of chronic hepatitis B have been described as having a poor prognosis. We have conducted a randomized controlled trial to assess the efficacy of lymphoblastoid interferon-alpha in 60 patients with antibody to HBeAg and hepatitis B virus DNA-positive chronic hepatitis. Patients received 5 million U/m2 interferon three times a week for 6 mo, or no treatment. Final evaluation 18 mo after randomization showed hepatitis B virus DNA negativity and ALT normalization in 53% of treated patients and in 17% of controls (p less than 0.01). The probability of sustained hepatitis B virus DNA loss was significantly higher in treated patients than in controls (p less than 0.005). Blinded histological assessment revealed improvement in 50% of treated patients compared with 33% of controls. Pretreatment hepatitis B virus DNA and aminotransferase levels and histological appearance were not predictive of response. The results of this trial indicated that marked reduction of viral replication in serum and remission of liver damage can be obtained with lymphoblastoid interferon in about 50% of patients with HBeAg antibody- and HBV DNA-positive chronic hepatitis. This rate of response is higher than that reported previously.
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PMID:A randomized controlled trial of lymphoblastoid interferon-alpha in patients with chronic hepatitis B lacking HBeAg. 155 34

Seven carriers of the Hepatitis B surface antigen who had acquired a form of chronic hepatitis D in the recent past were treated with lymphoblastoid alpha interferon (IFN) (10 MU three times weekly for 4 months, 6 MU three times weekly for other 8 months, with a 12 month follow-up after treatment). At the beginning of the study, these patients had a chronic active hepatitis with intrahepatic hepatitis D antigen but without signs of cirrhosis. By the end of therapy, five had normal amino-transferases and no trace of HDV-RNA in the serum. In two patients the liver enzymes and viremia relapsed during follow up; biochemical and virologic remission persisted after discontinuation of therapy in the other three patients. In the early non-cirrhotic stage of chronic hepatitis D, IFN may play a more consistent therapeutic role than in the average advanced case of the disease. Cytokine should be used as soon as a diagnosis of progressive hepatitis D is reached.
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PMID:Treatment of early chronic delta hepatitis with lymphoblastoid alpha interferon: a pilot study. 156 48

Alpha-interferon (IFN) has been used to treat hepatitis B virus carriers with chronic hepatitis Delta virus superinfection. Although the drug inhibits hepatitis Delta virus replication during administration, long-term clearance of the virus has not been obtained in most patients. The effectiveness of alpha-interferon on chronic HDV infection is therefore questionable. No data are available on acute infection. We report the case of a young, immunocompetent HBsAg carrier in whom hepatitis Delta virus superinfection occurred while he was receiving alpha-interferon in order to reduce high level HBV replication, and followed a peculiar course.
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PMID:Hepatitis delta superinfection during alpha-interferon treatment for hepatitis B. 157 75

It is well known that several inflammatory cytokines can modulate hepatocellular gene expression in a complex physiological process known as the hepatic acute-phase response. Since hepatitis B virus (HBV) characteristically induces a vigorous lymphomononuclear inflammatory response in the liver during acute and chronic hepatitis, it is possible that hepatocellular HBV gene expression may also be modulated by one or more of the cytokines produced by these cells. Using bacterial lipopolysaccharide (LPS) as a surrogate inducer of inflammatory cytokines in vivo, we have tested this hypothesis in a transgenic mouse model system. In experiments with two independent transgenic mouse lineages that express the HBV envelope region under the control of either HBV or cellular promoters, we observed a 50 to 80% reduction in the hepatic steady-state content of a 2.1-kb HBV mRNA following administration of a single intraperitoneal dose of LPS. The regulatory influence of several inflammatory cytokines known to be induced by LPS was also examined in this system. The negative regulatory effect of LPS was consistently reproduced by the administration of a single nontoxic dose of tumor necrosis factor alpha, and it was occasionally observed following the administration of high doses of alpha interferon and interleukin-6, while no effect was detectable in response to high-dose interleukin-1 alpha or to gamma interferon. These observations suggest that tumor necrosis factor alpha and perhaps other cytokines may activate a heretofore unsuspected intracellular pathway that negatively regulates HBV gene expression. The intracellular mechanism(s) responsible for this effect and its pathophysiologic relevance remain to be elucidated.
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PMID:Tumor necrosis factor alpha negatively regulates hepatitis B virus gene expression in transgenic mice. 158 37

The heterogeneity of hepatitis B virus (HBV) pre-S sequences coding for envelope proteins was tested by DNA amplification and direct sequencing of viral genomes from sera of 22 unselected chronic carriers resident in Southern Italy. The sequences of the dominant viral genome populations from 15 carriers were very similar to known published "wildtype" HBV genomes and showed no deletions. In contrast, in the HBV populations of six patients, deletions in the pre-S region, mainly clustered at the amino terminal end of the pre-S2 region, were found. Four of these mutant genome populations and those from another patient cannot express pre-S2 proteins due to deletions or a mutation of the translation initiation codon. Emergence of the pre-S mutant viruses either during the natural course of infection or after interferon treatment was found in follow-up sera of one and two patients, respectively. These data indicate a high prevalence of pre-S mutant viruses which cannot express pre-S2 and normal-size pre-S1 proteins. This has important implications for the usefulness of diagnostic pre-S protein assays and possibly for interferon treatment and the efficacy of new vaccines containing pre-S proteins.
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PMID:Hepatitis B virus genomes that cannot synthesize pre-S2 proteins occur frequently and as dominant virus populations in chronic carriers in Italy. 158 62

The relationship between the behavior of hepatitis B virus (HBV) replication markers and the response to treatment with recombinant alpha-2b interferon (IFN) was investigated in 11 patients with chronic hepatitis. At the end of 6 months of treatment, 4 patients showed a complete response to IFN: 2 more patients had seroconversion to HBeAb after 8 and 9 months of follow-up, respectively. The response to IFN was partial in the remaining patients. Pre-treatment levels of HBV DNA in patients showing complete response were lower than pre-treatment levels in patients with partial response: in addition, serum HBV DNA clearance during the treatment was associated with sustained remission more frequently than changes in the HBeAg/HBeAb system.
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PMID:Relation of changes in hepatitis B virus replication markers to the outcome of interferon treatment in patients with chronic hepatitis. 162 52


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