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)

Patients with non-A, non-B post-transfusion hepatitis were followed from the onset of their disease until their blood tests normalized, until they died, or until the present time. Of 66 patients, 30 had a spontaneous resolution of their biochemical disease. Ten patients died or were begun on immunosuppressive therapy with transaminases still abnormal. The remaining 26 patients had abnormal transaminase levels when last seen. By actuarial analysis, only 54% of hepatitis patients are predicted to develop s spontaneous biochemical remission within 3 yr. No further resolutions have occurred after that time, Icteric and anicteric acute disease may be equally likely to progress to chronic disease. Initial and follow-up liver biopsy specimens have revealed both chronic persistent and chronic active hepatitis. Two patients showed histologic evidence of cirrhosis, and a third developed a hepatic coagulopathy and sphenomegaly. No other patient to date, however, has veveloped overt evidence of hepatocellular failure or portal hypertension. Thus, non-A, non-B post-transfusion hepatitis frequently results in biochemical evidence of chronic liver disease, and in a few patients cirrhosis may develop slowly and in a clinically inapparent fashion.
 ...
PMID:The long-term course of non-A, non-B post-transfusion hepatitis. 677 6

The frequency and prognostic value of the "e" system was determined in acute and chronic hepatitis patients and in blood donors by immunodiffusion on Abott rheophoresis plates. The incidence of HBe Ag in acute viral hepatitis was 20% at the beginning of the disease; its persistance indicated a prolonged evolution and a tendency to a chronic course. The presence of anti-HBe at the beginning of the acute disease may indicate the onset of a non-B hepatitis in an HBe carrier. In chronic hepatitis the incidence of HBe Ag was 58% and in blood donors only 6%. Anti-HBe was absent in chronic hepatitis and present in 15% of blood donors.
 ...
PMID:[Frequency and prognostic value of the "e" system in hepatitis B virus infection]. 743 16

Mice infected with the neurotropic JHM strain of mouse hepatitis virus (MHV-JHM) develop a demyelinating encephalomyelitis several weeks after infection. Astrogliosis and infiltration of inflammatory cells are prominent findings in the brains and spinal cords of infected mice. In this report, astrocytes in infected spinal cords were analyzed for expression of three pleiotropic cytokines, TNF-alpha, IL-1 beta, and IL-6; Type 2 nitric oxide synthase (iNOS); and MHC class I and II antigen. The data show that all three cytokines and iNOS are expressed by astrocytes in chronically infected spinal cords. These activated astrocytes are localized to areas of virus infection and demyelination, although most of the astrocytes expressing these proteins are not MHV-infected. MHC class I and II antigen can be detected in these spinal cords as well, but not in cells with the typical morphology of astrocytes. TNF-alpha, IL-6, and iNOS are also evident in the brains of mice with MHV-induced acute encephalitis, but in marked contrast to the results obtained with the chronically infected mice, most of the cells expressing these cytokines or iNOS had the morphology of macrophages or other mononuclear cells and very few appeared to be astrocytes. Additionally, astrocytes and, most likely, oligodendrocytes are infected in the spinal cords of mice with chronic demyelination. These results are consistent with a role for both viral infection of glial cells and high localized levels of proinflammatory cytokines and nitric oxide in the demyelinating process in mice infected with MHV-JHM. They also show that analogously to the human demyelinating disease, multiple sclerosis, astrocytes are a major cellular source for these cytokines in mice with chronic, but not acute disease.
 ...
PMID:Activation of astrocytes in the spinal cord of mice chronically infected with a neurotropic coronavirus. 749 73

Twenty-five patients with post-transfusional C hepatitis have been tested retrospectively by IIIrd generation Recombinant Immuno Blot Assay (RIBA) in order to evaluate long-term anti HCV antibodies dynamics. The test was performed 1, 15, 70 and 140 days after the onset of the disease. Fifteen patients recovered and 10 became chronic. In the 15th day anti C33 and anti C22 were found in 76% of subjects, anti NS5 in 68% and anti C100 in 32%. In the 70th day, 96%, of patients had anti C22, 92% had anti C33 and anti NS5 and 52% showed anti C100. In the 140th day, all patients were positive for anti C33, and C22 and anti NS5, while anti C100 was present in 64%. Five-six years after the acute disease, all chronically progressed patients had a complete antibody pattern by RIBA III, while anti C22 was the only positive persisting antibody, among the recovered patients. Anti C22, anti C33 and anti NS5 shorten the serological "window-phase" during acute hepatitis, but no further improvement in diagnostic precocity seems to be guaranteed by third generation RIBA. The precocious appearance of complete RIBA III pattern during acute hepatitis may represent a herald for a chronic evolution of the disease.
 ...
PMID:[Long-term study of anti-HCV reactivity using 3d generation recombinant immunoblot assay in acute post-transfusion hepatitis]. 750

Neurotropic strains of mouse hepatitis virus (MHV) have been used extensively for the study of viral pathogenesis in the central nervous system (CNS), serving as models for human neurological diseases such as multiple sclerosis (MS). MHV strains A59 and JHMV both cause acute and chronic encephalomyelitis and demyelination in susceptible strains of mice and rats. In acute disease, CNS damage is most likely the result of lytic infection in neurons and oligodendrocytes, and death can be prevented by the adoptive transfer of Class I-restricted CD8+ T cells. However, in later stages of the disease induced by some MHV strains, virus tends to be restricted to astrocytes in a nonlytic infection, and the immune response appears to contribute to CNS damage. These data lead us to suggest that the astrocyte may play a central role in the neuropathogenesis of MHV infection. Consistent with this possibility, A59 has been reported to induce the expression of Class I molecules of the major histocompatibility complex (MHC) in glial cells following infection in vivo and in vitro. In this communication, we have examined the influence of persistent infection by both A59 and JHMV on MHC Class I expression in primary murine astrocytes. Persistence was characterized by the presence of intracellular viral antigen and mRNA in the absence of detectable infectious virus particles. Under these conditions, JHMV, but not A59, inhibited constitutive expression of the H-2 Kb molecule, with the magnitude of inhibition increasing with postinfection time. A59 was not able to induce Class I during persistence, presumably due to the lack of infectious virus particles. Class I expression was restored by the addition of gamma-interferon (IFN-gamma) to astrocytes persistently infected with either A59 or JHMV. Thus, Class I inhibition is not a permanent consequence of JHMV persistence, and persistence does not interfere with normal signalling pathways for Class I induction.
 ...
PMID:Effect of persistent mouse hepatitis virus infection on MHC class I expression in murine astrocytes. 771 17

Viral pathogenicity is a result of an imbalance between viral replication and the host's immune defences. When the virus is lymphotropic, understanding the pathogenic process of the viral disease becomes complicated because virus/lymphocyte interactions can alter the cell's integrity and subsequently induce immunodeficiency. The immune system plays an important role in the outcome of acute disease induced by the mouse hepatitis virus type 3 (MHV3). The use of attenuated escape mutants provides a tool to study the role of viral properties involved in its pathogenicity. We selected MHV3 mutants by virtue of their resistance to neutralization by monoclonal antibodies (mAb), in order to study their pathogenic properties. We reported that two MHV3 escape mutants were attenuated in their pathogenic properties according to inoculation site and with regard to survival time and ability to deplete T- and B-cell subpopulations in the spleen, thymus and bone marrow of susceptible Balb/c mice. The highly attenuated CL12 mutant could not induce depletion in T or B cells following intraperitoneal (i.p.) or intranasal (i.n.) inoculations, at three days postinfection. The less attenuated 51.6 mutant, however, maintained the ability to deplete T and B cells following i.p. inoculation, as described with the pathogenic MHV3. In contrast, no depletion of T cells following i.n. inoculation was induced with this mutant, although B lineage cells decreased. The use of such mutants enabled us to examine the role of each compartment of the immune system, since the highly attenuated CL12 mutant induced no immunodeficiency, as defined by immune cell depletion, whereas the less attenuated 51.6 mutant maintained its ability to decrease only the B-cell compartment after i.n. inoculation. Results are discussed with regard to the virus/lymphocyte interactions during the pathogenic process.
 ...
PMID:Pathogenicity of neutralization escape mutants of mouse hepatitis virus: correlation with T- and B-cell depletions. 775 1

For two reasons hepatitis B virus infection is an important problem in patients with cancer. First, multidrug cancer chemotherapy may reactivate or worsen a previously benign chronic HBV infection. Second, patients undergoing cancer chemotherapy are at an increased risk of acquiring and spreading HBV which may result in an endemic infection. HBV reactivation may precipitate into a severe acute disease including fulminant hepatitis. In contrast, the acquisition of HBV during cancer chemotherapy commonly takes a mild clinical course but frequently leads to persistently high viremia. This state of immunotolerance to viral antigens allows viral replication without any sign of liver cell destruction. Withdrawal of chemotherapy does not cause significant changes if infection occurred during cytotoxic chemotherapy. Infection with HBV during cancer chemotherapy, therefore, may be considered as a model of an induced antigen-specific immunotolerance. In agreement with this hypothesis, vaccination against HBV during cancer chemotherapy does not prevent spread of HBV in oncology wards as it does not produce significant anti-HBs titers. Furthermore, vaccination even suppresses the immune response to later booster doses after chemotherapy has been withdrawn.
 ...
PMID:Clinical and immunological aspects of hepatitis B virus infection in children receiving multidrug cancer chemotherapy. 826 Aug 57

Granulomatous hepatitis as the sole manifestation of acute Q fever has been reported only rarely, although minimal hepatic dysfunction may be common in the acute disease. In this paper we report two patients with acute Q fever who presented with hepatitis; one of whom had granulomatous hepatitis on liver biopsy. We discuss the serological diagnosis of acute and chronic Q fever particularly in relation to hepatitis.
 ...
PMID:Coxiella burnetii serology in granulomatous hepatitis. 803 4

Liver disease caused by hepatotrophic viruses imposes a substantial burden on health care resources. Persistent infections from hepatitis B virus (HBV), hepatitis C virus, and hepatitis delta virus result in chronic liver disease, while hepatitis A virus and hepatitis E virus produce a self-limited disease. Effective hepatitis B vaccines that provide long-term protection against chronic HBV infection have been available for > 10 years, while inactivated hepatitis A vaccines have recently been shown to prevent acute disease. To prevent transmission of HBV, scientifically and epidemiologically sound recommendations call for vaccination of all infants in successive birth cohorts worldwide. For hepatitis A vaccines, recommendations will be developed in the near future and should reflect vaccine performance and the epidemiology of hepatitis A. A number of policy, health care financing, and educational issues must be addressed to ensure the effective use of both of these vaccines.
 ...
PMID:Prevention of acute and chronic liver disease through immunization: hepatitis B and beyond. 851 36

The morphology of autoimmune hepatitis is characterized by portal-periportal predilection of necroinflammatory lesions. In comparison to the viral type of hepatitis severe piece-meal-necroses, the collapse of periportal parenchyma, and to a higher degree acinar transformation of hepatocytes are more prominent. The autoimmune hepatitis may start with acute disease displaying unusual clinical und histopathologic features. The postinfantile giant cell hepatitis seems to constitute a variant of autoimmune hepatitis. Autoimmune hepatitis has been reproduced in animal models and it could be demonstrated in rabbits that humoral immunity plays a role in tissue damage. The importance of cellular mechanisms could be analyzed in syngenic mice showing that the CD4-positive lymphocytes play a pivotal role. The most promising candidate antigen seems to be the asialoglycoprotein-receptors including the liver specific protein (LSP). By immunohistologic analysis dense deposits of IgG could be demonstrated in sinusoids and on the membranes of hepatocytes. In accordance with in vitro data the determination of CD4 positive lymphocytes in the tissue was found to play a decisive role in cellular immune reaction. The HSP65 molecule seems to evoke mechanisms that have been shown to play a pathogenetic role in experimental arthritis.
 ...
PMID:[Autoimmune hepatitis]. 860 Jun 83


<< Previous 1 2 3 4 5 6 7 8 Next >>