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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis may be caused by hepatitis A virus, hepatitis B virus, hepatitis C virus (classic non-A non-B viral hepatitis), hepatitis D virus (delta agent), and hepatitis E virus (epidemic non-A non-B viral hepatitis). Cytomegalovirus, Epstein-Barr virus, and herpes simplex virus may also occasionally cause hepatitis. Some forms of hepatitis carry the risks of chronic infection, cirrhosis, or hepatocellular carcinoma. Treatment options for viral hepatitis are limited and, in many cases, still under investigation. Prophylaxis is available for many forms of hepatitis and should be offered to those at risk.
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PMID:Viral hepatitis. The new ABC's. 212 Jun 86

The major cause of chronic post-transfusion hepatitis, the hepatitis C virus (HCV), has been identified. HCV is a single-stranded linear RNA virus with characteristics similar to the flaviviruses. A different agent, the hepatitis E virus, is associated with epidemic (enterically-transmitted) non-A, non-B hepatitis. At present, infection with HCV is recognized by the finding of anti-HCV antibodies, positive in up to 90% of patients with chronic non-A, non-B post-transfusion hepatitis. Antibodies to HCV are detected in 1% of normal volunteer blood donors and in the majority of donors implicated in post-transfusion hepatitis. HCV antibodies are also found in patients with autoimmune liver disease and hepatocellular carcinoma. Moreover, HCV infection may contribute to the pathogenesis of liver disease in alcoholic patients. The role of HCV infection in fulminant non-A, non-B hepatitis and hepatitis-associated aplastic anemia has not been elucidated as yet. Therapy of chronic non-A, non-B hepatitis with recombinant human alpha-interferon has been shown to improve or normalize aminotransferase levels in approximately 50% of patients, most of whom have evidence of HCV infection. However, relapse after cessation of treatment is common. In the future, screening blood for evidence of HCV infection may prevent most cases of non-A, non-B post-transfusion hepatitis.
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PMID:Hepatitis C. 215 11

Small 'featureless' viruses (less than 50 nm) are difficult to identify by routine immune electron microscopy techniques, particularly when they are mixed with debris from stool or cell culture extracts. A combination of conventional immune electron microscopy (IEM) and solid phase IEM (SPIEM) methodologies was used to identify hepatitis A virus (HAV) in stool and cell culture extracts and non-A non-B hepatitis (hepatitis E) in stool extracts. Compared with conventional IEM, the modified SPIEM method resulted in a significant increase in the number of particles observed. Several small aggregates, each containing 2-20 particles, were observed scattered randomly within most grid squares. Similar results were seen with stool extracts from hepatitis E (HEV) infections. The SPIEM method is a simple, highly sensitive specific assay that facilitates rapid identification of enteric hepatitis viruses. Several experiments were done to characterize the effects of altered physical environment within the assay and to evaluate potential modifications.
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PMID:Identification of enterically transmitted hepatitis virus particles by solid phase immune electron microscopy. 217 64

In earlier studies, hepatitis E virus (HEV) particles were detected in the stools of patients with enterically transmitted non-A, non-B (ENANB) hepatitis, and HEV was etiologically associated with this disease. Such particles have not been observed in the liver, however. We describe the pathological findings in the liver of a young pregnant woman from Nepal who died as a result of fulminant NANB hepatitis. IgM antibody to HEV was detected in the patient's serum by immune electron microscopy, suggesting that she was acutely infected with that virus. On light microscopic examination of the liver we observed cholestatic hepatitis with proliferation of bile ductules and pseudoglandular arrangement of hepatocytes around distended bile canaliculi. Three types of virus-like particles were detected by electron microscopy. The most frequently observed particles were in cells lining small bile ductules; they measured 32-37 nm and were enclosed by a membrane. Particles of a second type were seen in clusters in the sinusoidal cells; they were uniform in size, without a membrane, and measured about 32 nm in diameter. Particles of a third type (65 nm) were found in epithelial cells of the small bile ductules. Among the particles we detected, the 32 nm particles most closely resembled those of HEV.
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PMID:Virus-like particles in the liver of a patient with fulminant hepatitis and antibody to hepatitis E virus. 239 10

Serologic markers of hepatitis B virus (HBV), including HBV DNA, and of hepatitis delta virus were measured in three villages in Gabon. Of 303 subjects studied, 19% were carriers of hepatitis B surface antigen (HBsAg); 8.5% of these had anti-delta antibodies. No difference among the three villages was observed. All HBV DNA carriers were children less than 11 years of age. In the 2-9-year-old group, 71% of the HBsAg-positive children tested were HBV DNA carriers. These results indicate that HBV prevalence is high in Gabon and emphasize the importance of horizontal transmission of HBV in Africa. Antibodies to hepatitis C virus, assessed in one of the three villages, were found with a prevalence of 35% with a second generation enzyme-linked immunosorbent assay (ELISA) and 24% with a third generation ELISA. None of 35 subjects tested for antibodies to hepatitis E virus was positive.
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PMID:Hepatitis B, C, D, and E markers in rural equatorial African villages (Gabon). 748 84

During 1990, 38 patients with fulminant non-A, non-B hepatitis (NANB) died in Government Medical College Hospital, Aurangabad. Serum samples from these patients were tested for antibodies to hepatitis C virus (anti-HCV) and IgM antibodies to hepatitis E virus (IgM-anti-HEV). All samples were also subjected to polymerase chain reaction (PCR) for the detection of HBV DNA, HCV RNA and HEV RNA. None of the patients had circulating anti-HCV antibodies; three had HCV RNA. Based on anti-HEV-IgM positivity 14 patients (37%) could be diagnosed as suffering from hepatitis E. None was positive for HEV RNA. In the absence of serological markers, HBV DNA was present in three cases. None of the HBV DNA positive patients had anti-delta antibodies. Dual infections (HBV with HEV, and HBV with HCV) were seen in two cases. The aetiology of half of the NANB cases could not be assigned to the known hepatitis viruses using current techniques.
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PMID:Contribution of HEV and HCV in causing fulminant non-A, non-B hepatitis in western India. 748 46

Hepatitis E virus (HEV) is a polyadenylated, positive-stranded RNA virus which is a major cause of enterically transmitted non-A, non-B hepatitis in many developing countries. The viral genome contains three different open reading frames (ORFs): ORF1, which is believed to encode nonstructural proteins, and ORF2 and ORF3, which are believed to encode structural proteins. The full-length putative structural proteins encoded by ORF2 and ORF3 of HEV have been cloned and expressed in recombinant vaccinia virus. Proteins encoded by ORF2 and ORF3 when expressed in vaccinia virus are recognized by pooled sera obtained from individuals with acute hepatitis E. Vaccinia-expressed viral gene products of HEV will have utility in characterizing the cell-mediated immune response to HEV.
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PMID:Expression of hepatitis E virus putative structural proteins in recombinant vaccinia viruses. 749 58

Hepatitis E virus (HEV), the causative agent of enteric non-A, non-B hepatitis, is a positive-stranded RNA virus. Because of the virus's inability to grow in culture, several nonhuman primates have been used for the propagation of HEV. Using strand-specific reverse transcription-polymerase chain reaction (RT-PCR), we demonstrate the presence of negative-stranded HEV RNA replicative intermediates in the livers of infected animals. This constitutes the first direct evidence of HEV replication in the liver of the infected animals and reinforces the validity of such a model to study HEV infection, disease pathogenesis, and immunity.
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PMID:Detection of the negative strand of hepatitis E virus RNA in the livers of experimentally infected rhesus monkeys: evidence for viral replication. 751 19

Hepatitis E is endemic in developing countries and may occur as imported hepatitis in industrialized countries. A 46-year-old Japanese man developed immunoserologically diagnosed acute hepatitis E in Japan 4 months after he had made a trip to China. He had bought a Chinese herbal medicine there, taking it occasionally until approximately 6 weeks prior to the onset of acute hepatitis. Nucleotide sequencing of the 3' terminal region of the viral cDNA amplified from the patient's serum by polymerase chain reaction revealed a high degree of homology (99.8% of 752 nucleotides) with the Chinese strain. Thus, the results of sequencing suggest that his hepatitis E was caused by infection with the Chinese strain, via the Chinese herbal medicine.
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PMID:Hepatitis E probably contracted via a Chinese herbal medicine, demonstrated by nucleotide sequencing. 755 Aug 68

From 1981 to 1993, 40 cases of acute type A viral hepatitis were reviewed and 2 cases (5%) of relapsing hepatitis were reported here. One case relapsed two weeks after remission and the other relapsed three weeks after remission, both had benign courses and recovered within four months. They were negative for serum hepatitis B surface antigen and hepatitis B core IgM antibodies. The serum autoantibodies, hepatitis C antibodies and hepatitis E antibodies were all negative during relapse. In summary, relapsing hepatitis A is rare in Taiwan and it is not related to multiple viral infections.
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PMID:Acute relapsing hepatitis A in Taiwan--a rare event not related to multiple viral infection: a report of two cases. 755 20


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