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

The interferon treatment of chronic viral hepatitis leads to a measurable inhibition of replication of the various hepatitis viruses. In adult patients with chronic HBe-Ag-positive hepatitis B, the seroconversion rate is tripled by therapy when compared with untreated controls. In chronic hepatitis C, biochemical remission is achieved in about 50% of patients, but there is a high tendency to relapse. Interferon treatment has little effect in hepatitis B virus infection transmitted perinatally and in chronic delta hepatitis. Better knowledge of prognostic variables and deeper insights into the mechanisms of chronic hepatitis C virus infection should help both to increase rates and duration of remissions and to reduce the rates of relapse in the future.
 ...
PMID:[Interferon treatment of chronic viral hepatitis]. 137 40

2,346 liver samples from 17 cities of China for intrahepatic hepatitis D antigen (HDAg) were studied by direct enzyme-labelled technique. HDAg was detected in 167 out of 1,764 samples of HBsAg positive individuals making a detection rate of 9.47%. Hepatitis D virus (HDV) infection existed in all the examined districts with no significant difference in the HDAg detection rate. It was found that the intrahepatic HDAg detection rate was related to the pathologic type of the liver disease. The HDAg detection rate in chronic liver diseases and severe hepatitis was higher than in other liver diseases. It suggests that HDV infection is associated with the progression and chronicity of the liver disease. Studies on the relationship between HDV infection and HBV replication showed that HBV replication might be suppressed by HDV infection. Both HDV and HBV, however, could replicate in the same hepatocyte simultaneously.
 ...
PMID:Hepatitis D virus infection in liver tissues of patients with hepatitis B in China. 139 39

From June 1985 to June 1989, sera from 425 cases of acute viral hepatitis were gathered from 2 hospitals in Bombay; 331 sera were positive for hepatitis B surface antigen and immunoglobulin M anti-hepatitis B core antigen, and the donors' disease was diagnosed as hepatitis B. Anti-hepatitis D virus was found in 124 of these sera, and hepatitis D antigen was present in 24 more, conclusively proving the presence of hepatitis delta infection in association with hepatitis B in Bombay. Among the 425 cases of hepatitis, 39 cases of fulminant hepatitis developed, of whom 31 died. Hepatitis B virus (HBV) was the apparent viral infection in 32 of the fulminant cases, and 20 (63%) of them also showed evidence of hepatitis D virus (HDV) infection, suggesting an aggravation of their clinical course due to concurrent HBV and HDV infections.
 ...
PMID:Hepatitis delta virus infection in Bombay. 144 Aug 25

Serial liver biopsy specimens from 11 patients who had liver transplants after hepatitis D virus (HDV)-related end-stage liver disease developed were examined, allowing a novel opportunity to study the evolution of HDV infection in relation to hepatitis B virus (HBV) infection from the earliest stages. Hepatitis D virus antigen was detected in liver tissue in the absence of either tissue or serologic evidence of HBV recurrence within 3 months in all eight patients biopsied at that time. After serologic evidence of recurrent HBV infection in nine patients, there was a massive increase in hepatic expression of hepatitis D virus antigen and this was associated with the transient appearance of serum hepatitis D virus antigen in four patients. Coexpression of both HBV and HDV antigens in the liver was associated with the onset of lobular hepatitis, which progressed to chronic hepatitis in five patients. These findings indicate that HDV can survive and synthesize HDAg in the absence of detectable HBV, but when HBV replication increased to a detectable level, HDV replication was enhanced massively. Contrary to current thinking, the data suggest that HDV is not directly cytopathic and that HBV is an essential cofactor in the evolution of hepatocellular damage.
 ...
PMID:Evidence that hepatitis D virus needs hepatitis B virus to cause hepatocellular damage. 146 51

Four patients who received an auxiliary partial liver graft for decompensated liver cirrhosis due to hepatitis B (HBV), associated in two cases with hepatitis D virus (HDV) superinfection, were studied. The sequential appearance of hepatitis B and D antigens in the grafts was investigated in serial liver biopsies by immuno-histochemical methods and compared with the viral antigenic profiles of the host livers. The histological changes in the liver grafts were studied in relation to the viral expression patterns. One week after transplantation, expression of HBsAg was already apparent in two grafts. HBcAg was found in the graft of the only patient with HBcAg in the host liver. HDAg was expressed in the grafts of both patients with HDV superinfection; in one of these cases HDAg was present without HBsAg. At 3 months, viral antigen expression was maximal. Expression of HBsAg and HBcAg in the grafts of the two HDV-positive patients was, however, less extensive than in the two HBV-positive patients. All patients developed a mild lobular hepatitis, histologically demonstrated between the 47th and 107th posttransplantation day. In the two HBV-positive, HDV-negative patients, cirrhotic transformation of the graft occurred within 1 year. In the HDV-positive patients only a mild chronic active hepatitis with slight or moderate fibrosis was observed after 1 year. We conclude that recurrence of HBV and HDV infection in auxiliary liver grafts is demonstrable within 1-3 weeks. HBV infection in liver grafts may be a rapidly progressive disease. Coinfection with HDV does not aggravate the acute hepatitis and may even suppress the progression of chronic HBV.
 ...
PMID:Course of hepatitis B and D virus infection in auxiliary liver grafts in hepatitis B-positive patients. A light-microscopic and immunohistochemical study. 150 Jun 81

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.
 ...
PMID:Nosography and immunopathogenesis of viral hepatitis. 150 25

Parenterally shared blood and sexual transmission are the main routes of spread of hepatitis B in the United States. Most cases resolve spontaneously without specific treatment. Passive immunization provides temporary protection in certain postexposure settings. Active immunization achieves high protection rates. Duration of protection and the need for booster doses are not well defined. Many cases of fulminant B hepatitis, severe chronic active hepatitis, and end-stage cirrhosis secondary to hepatitis B are due to hepatitis delta virus infection. The delta virus requires the presence of hepatitis B for expression of disease. Hepatitis B prophylaxis should help eliminate delta hepatitis.
 ...
PMID:Viral hepatitis in the 1990s, Part II: Hepatitis B and delta virus. 152 72

A 39 years old homosexual male suffering from chronic type B hepatitis superinfected by HDV, and positive for anti-HIV1 was treated with zidovudine associated with high doses of recombinant interferon alpha for onset of an extensive cutaneous Kaposi sarcoma. Other than the long-lasting disappearance of Kaposi's lesions, this therapy was followed by complete recovery from hepatitis B and D. Serological and hepatic clearance of both viruses was marked by two successive cytolytic peaks separated by a 9 month interval. The patient's immunologic status has remained stable at 30 months. To our knowledge, such a success had never been reported in the literature and the clearance of both hepatitis B and D viruses in an AIDS patient stands in sharp contrast with the usual rapidly progressive evolution of those triple coinfections. This phenomenon illustrates the potential benefits of zidovudine in association with high dose of interferon alpha in HIV patients suffering from hepatitis D.
 ...
PMID:[Recovery of chronic hepatitis B- delta infection by zidovudine and recombinant interferon alpha combination therapy in a patient with Kaposi's sarcoma associated with HIV infection]. 152 1

Hepatitis delta antigen (HDAg) is the only known protein of hepatitis delta virus and was previously shown to localize in the nucleoplasm of infected liver cells. In this study, nuclear localization signals of HDAg were defined by expressing various domains of the antigen in both hepatic and nonhepatic cells as beta-galactosidase fusion proteins. A cytochemical staining assay demonstrated that a domain from amino acid residues 35 to 88 of HDAg was able to facilitate transport to the nucleus of the originally cytoplasm-localized protein beta-galactosidase. Two nuclear localization signals, NLS1 and NLS2, which are similar to those of simian virus 40 T antigen and polyomavirus T antigen, respectively, were identified. Either NLS1 or NLS2 alone was sufficient for the nuclear transport of HDAg. However, a fusion protein (N65Z) containing beta-galactosidase and the N-terminal 65 amino acids of HDAg, containing NLS1, was localized exclusively in the cytoplasm and perinuclear region. A possible hydrophobic subdomain between amino acid residues 50 and 65 may block the function of NLS1. Nevertheless, N65Z could enter the nuclei of transfected cells when it was coexpressed with full-length HDAg. Entry into the nucleus may be mediated by the coiled-coil structure rather than the putative leucine zipper motif located between amino acid residues 35 and 65. The existence of two independent nuclear localization signals may ensure the proper functioning of HDAg in the multiplication of delta virus in the nucleus. In addition, two putative casein kinase II sites (SRSE-5 and SREE-126) that may be important in controlling the rate of nuclear transport were found in HDAg.
 ...
PMID:Nuclear localization signals, but not putative leucine zipper motifs, are essential for nuclear transport of hepatitis delta antigen. 152 50

In carriers of HBsAg (Hepatitis B virus surface antigen) the incidence of Hepatitis D virus infection was studied in 72 (61.3%) males and 45 (38.5%) females, totally in 117 cases with a mean age of 34.8 years. There were 26 (22.2%) asymptomatic carriers of HBsAg where in other chronic carriers the diagnosis were as follows; 29 (24.7%) chronic persistent hepatitis, 20 (17.0%) chronic lobular hepatitis, 23 (19.6%) chronic active hepatitis and 19 (16.2%) posthepatic cirrhosis. The incidence of HDV serologic markers were found to be positive in 19 (16.2%) out of 117 cases.
 ...
PMID:[Incidence of hepatitis D virus infection in chronic hepatitis B virus carriers]. 152 42


1 2 3 4 5 6 7 8 9 10 Next >>