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 histologic appearances characteristic of chronic active hepatitis (CAH) were observed in liver biopsies of seven patients among whom alcohol abuse was the only identifiable determinant of liver disease. Clinical, hematologic, biochemical and histologic features in these patients were contrasted with those of 20 patients with typical alcoholic hepatitis. For the CAH group, the liver was less enlarged below the costal margin, a palpable spleen was more frequent, the mean neutrophil count was lower, and there was a lower mean level of transaminase enzymes. In both groups there was minimal evidence of the serologic markers of autoimmune CAH or antecedent hepatitis B virus (HBV) infection. Histologically, all liver biopsies in the CAH group showed perilobular "piecemeal" necrosis, "rosette" formation and dense portal and septal lymphoid infiltrates, in contrast to the fatty change, Mallory bodies and intralobular neutrophil clusters of the alcoholic hepatitis group. In the CAH group, a second liver biopsy was assessed after a period during which alcohol consumption was known; histologic improvement or deterioration correlated with abstinence or continuation of drinking. Thus "alcoholic" CAH has some clinical and histologic features distinct from those of typical alcoholic hepatitis, but the two types were similar in other respects including dependence of the course of disease on continuing use of alcohol.
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PMID:Chronic active hepatitis in alcoholic patients. 664 17

With a monoclonal antibody which reacts with all HLA class 1 antigens it was found that these antigens are not uniformly distributed in all nucleated cells. Rather HLA class 1 antigens are restricted in their distribution to lymphoid cells, endothelial cells of small vessels, and certain epithelia including mammary duct cells. These antigens were not detected on hepatocytes, specialised cells of the central nervous system, or on the tumour cells of 8 out of 17 human mammary cancers. Given the hypothesis that T cells only respond to foreign antigens on cells which share a common major histocompatibility antigen, these results imply that the T cell responses to viral infections of hepatocytes--for example, hepatitis B virus and the CNS--for example, subacute sclerosing encephalitis, are mediated through an antigen system other than HLA class 1. The absence of HLA class 1 antigen on many mammary cancer cells may be of prognostic significance if T cell modulation of tumour growth is mediated through this class of antigens.
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PMID:Distribution of HLA class 1 antigens in normal human tissue and in mammary cancer. 702 3

The course of experimental hepatitis B in chimpanzees was studied, and two biochemically, serologically, and histopathologically distinctive types were identified. The first type was self-limiting, rapidly resolving hepatitis with spiking and short-term elevation of SGPT starting at around 5 weeks after the appearance of HBs antigenemia. The second type was smoldering and persistent hepatitis with low-plateau-forming persistent transanimase abnormality developing around 10 weeks after the appearance of HBsAg. Anti-HBc became positive before the transaminase elevation in the second type, while in the first type it became positive after the SGPT elevation. Histologically, the second type was characterized by marked infiltration of lymphoid cells in portal areas with lymphoid follicles. This was seen even before the histologic manifestations of liver cell injury and the elevation of SGPT in two cases. The portal inflammatory cell infiltration became evident at 6 to 9 weeks after the HBsAg appearance and became increasingly more severe thereafter. The intralobular changes remained mild, with rare liver cell necroses. Chronic hepatitis developed subsequently in two cases. In the first type, the portal changes developed almost simultaneously with intralobular changes and were not prominent. In contrast to the second type, the intralobular changes with multiple liver cell necrosis were more severe.
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PMID:Two distinct types of hepatitis in experimental hepatitis B virus infection. 737 87

A morphological investigation was carried out to study the pathological features of liver cirrhosis caused by hepatitis C virus (HCV) infection. The materials consisted of liver specimens taken from 47 cases of anti-HCV antibody-positive liver cirrhosis (37 by surgery for hepatocellular carcinoma and 10 by autopsy), and from 21 cases of hepatitis B surface antigen-positive liver cirrhosis as the control. Liver specimens containing more than 10 regenerative nodules were examined. In addition, a histometric study was conducted to determine the degree of fibrosis and the size of regenerative nodule using a computer image-analysis system. The results showed that the histological characteristics of HCV antibody-positive liver cirrhosis are: (i) broadly expanded fibrous septa and small regenerative nodules; (ii) relatively strong inflammatory reaction and prominent lymphoid aggretation in the fibrous septum; and (iii) mild regenerative activity of the liver parenchyma, and infrequent liver cell dysplasia. These findings may facilitate better understanding of the pathology of HCV antibody-positive liver cirrhosis and more accurate pathological diagnosis by needle biopsy.
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PMID:Pathomorphological study of HCV antibody-positive liver cirrhosis. 753 51

The pathogenesis and perpetuation of hepatocellular injury in hepatitis C viral infection remains unclear. It has been proposed that a direct viropathic effect, the host immune response, or both mediate cell damage. To address this issue, the immunophenotype of the inflammatory infiltrate in the liver of 18 patients with abnormal liver function tests and serologically detectable hepatitis C virus antibodies was compared with seven control patients (three cases with hepatitis B virus infection, two with alcoholic hepatitis, and one patient each with primary biliary cirrhosis and autoimmune hepatitis). The immunohistochemical markers included UCHL1, L26, Ham-56, Mac-387, CD68, Leu-M1, and cathepsin B. We found that T cells represent the predominant cell type in both histopathologic patterns of hepatitis C, ie, chronic active hepatitis and chronic persistent hepatitis, but the intensity of the T-cell infiltrate displayed marked differences. B-cell infiltrates were only seen in the germinal centers of lymphoid follicles in portal tracts. Furthermore, significant numbers of CD68-positive macrophages/monocytes were seen in the more aggressive form of hepatitis C viral infection. These data suggest that the T-lymphocyte-mediated host immune response is similar in chronic active and chronic persistent hepatitis patterns of hepatitis C viral infection, but varies in its intensity. In addition, macrophages/monocytes may play a role in hepatocyte and bile duct injury in chronic hepatitis C.
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PMID:Chronic hepatitis C. Analysis of host immune response by immunohistochemistry. 753 56

Two class I major histocompatibility complex (MHC) proteins with molecular masses of 43- and 39-kDa were identified in the cell surface membranes of normal woodchucks using a newly developed antiwoodchuck class I monoclonal antibody (mAb) B1b.B9 and immunoblotting. B1b.B9 was generated by immunizing mice with viable woodchuck peripheral blood mononuclear cells and was selected for anti-class I MHC reactivity using a cellular enzyme-linked immunoassay, indirect immunofluorescence on tissue sections and flow cytofluorimetry. The distribution pattern of class I MHC antigen on woodchuck lymphoid cells was found to be similar to that reported in other species. Also, the antigen expression on normal woodchuck hepatocytes was comparable to that observed on normal human liver parenchymal cells; thus, the antigen was not detected on hepatocytes by staining of liver tissue sections, but was found by indirect immunofluorescence staining of isolated liver cells. Western blot analysis of the plasma membranes from normal woodchuck hepatocytes revealed the presence of a single species of class I MHC heavy chain protein with a molecular mass of 43-kDa, whereas splenocyte plasma membranes showed intense expression of a 43-kDa species, as well as the presence of a 39-kDa protein. The 39- and 43-kDa proteins were extracted with Triton X-114 to the hydrophobic protein phase, suggesting that they both contain a hydrophobic transmembrane domain. The data obtained indicate that the B1b.B9 identifies a nonpolymorphic epitope of woodchuck class I MHC heavy chains, providing an important reagent for the study of the pathogenesis of hepatitis B virus infection in a woodchuck model.
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PMID:Identification of woodchuck class I MHC antigens using monoclonal antibodies. 765 41

Hepatitis C is usually poorly symptomatic, particularly in the acute phase. After an incubation period ranging from 5 to 12 weeks, the symptoms are nonspecific and icterus is rarely present. Laboratory results are more suggestive, showing characteristic fluctuations in transaminases comprising periods with normal values. Chronic hepatitis is probable when elevation of transaminases persists for more than 6 months. Chronic virus C hepatitis is usually asymptomatic. Clinical manifestations are poorly specific and transaminase concentrations are generally little increased and variable in over 75% of the cases. Some histological lesions are more often observed in the chronic stage, particularly steatosis, presence of intraportal lymphoid nodules and bile duct involvement. The natural history is dominated by the risk of development to cirrhosis and hepatocellular carcinoma. A course to chronic hepatitis C is observed in 20 to 70% of cases, while the risk of developing cirrhosis is between 10 and 38% within approximately 20 years. Prognosis is then linked to decompensation of cirrhosis and especially to the development of hepatocellular carcinoma, within approximately 10 years after appearance of cirrhosis, with a prevalence of at least 20%. The association of other factors such a hepatitis B virus or alcohol can accelerate this course.
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PMID:[Hepatitis C]. 772 19

The mechanisms of viral persistence are complex and include infection of the lymphoid cells. In the case of hepatitis B virus, early observations have suggested that HBV may infect peripheral blood mononuclear cells (PBMC). In animal models studies in chronic hepatitis B patients have further confirmed that viral DNA replicative intermediates, as well as viral transcripts and proteins, can be detected in PBMC under certain conditions. The consequences of this lymphotropism are not fully understood, but it seems likely that PBMC represent an extrahepatic reservoir of virus. The ability of hepatitis C virus to infect PBMC has been demonstrated in vivo and in vitro. The link between HCV lymphotropism and both the natural history of the viral infection and the immunological disorders frequently observed in HCV infections still needs to be established. In both cases, the infection of PBMC by HBV or HCV may represent the source of infection of the liver graft in patients transplanted for end-stage liver disease associated with HBV or HCV.
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PMID:Lymphotropism of hepatitis B and C viruses: an update and a newcomer. 778 5

Lubin et al recently described a new approach that enables the generation of human/mouse chimera by adoptive transfer of human peripheral blood mononuclear cells (PBMC) into lethally irradiated normal strains of mice, radioprotected with bone marrow (BM) from donors with severe combined immune deficiency (SCID). In the present study, we demonstrate in such human/mouse chimera a marked humoral response to recall antigen, such as tetanus toxoid (TT) or hepatitis B surface antigen (HBsAg), as well as a significant primary response to keyhole limpet hemocyanin (KLH). Maximal anti-KLH response in human/Balb chimera was attained 2 to 4 weeks after the immunization and declined thereafter. One week after transplantation, the predominant anti-KLH subtype was IgM, while after 2 weeks, the dominance had shifted to IgG. Similar primary antibody response was also demonstrated against the human immunodeficiency virus (HIV) Nef protein. Comparison between human/Balb and human/SCID chimera showed a major difference in their ability to mount a primary response against KLH. In Balb/c recipients, more than half of the mice exhibited marked IgM titers against KLH, while there was hardly any anti-KLH IgM response in the SCID recipients. From the earliest time point onwards, when anti-KLH antibodies were found in the latter chimera, they were predominantly of the IgG type. We have previously shown that in human/Balb chimera, unlike in SCID recipients, dissemination of transplanted PBMC into the spleen and other internal organs occurs within 24 hours. Therefore, it is likely that the early seeding in the appropriate microenvironment of the lymphoid tissues, is crucial for the maintenance of virgin human B cells.
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PMID:Human/mouse radiation chimera are capable of mounting a human primary humoral response. 779 48

Recent reports have shown that HCV infection is not only restricted to hepatocytes. Like hepatitis B virus (HBV), which also was thought to be strictly hepatotropic in early molecular and cellular investigations, infection of lymphoid cells by HCV in vivo has been demonstrated. We showed that total peripheral blood leukocytes of chronically HCV-infected patients are infected by detection of plus- and minus-stranded HCV RNA using strand-specific oligonucleotide primers in the RT-PCR. These cells also represent extrahepatic sites for the viral replication, as demonstrated by incorporation of [3H]-uridine into nascent RNA after stimulation of the cells with a mitogen. Furthermore, total PBML from an uninfected person could be infected in vitro using an HCV-positive serum. It could be shown that replication of HCV RNA takes place in these cells. Examination of different subsets of PBML showed predominant infection of B-lymphocytes during HCV disease. Additionally, infection of T-lymphocytes was detected in about 50% of all chronically HCV-infected patients.
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PMID:B-lymphocytes are predominantly involved in viral propagation of hepatitis C virus (HCV). 803 62


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