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

A 56-yr-old man was admitted for evaluation of fever, chills, jaundice, and alcoholic stools. Laboratory studies suggested a cholestatic process. Ultrasonography, computed tomography, and transhepatic cholangiography failed to reveal any abnormalities. Acute infection with Francisella tularensis was confirmed serologically, and a liver biopsy revealed cholestatic hepatitis with focal coagulative necrosis. Recovery was coincident with antibiotic therapy.
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PMID:Tularemic hepatitis presenting as obstructive jaundice. 352 44

Acute infection with Coxiella burnetii usually results in a self-limited illness, but it can occasionally cause chronic endocarditis or hepatitis. Headache is a common presenting symptom of acute infection with this agent, but specific neurological abnormalities are rare. We report the case of a patient with acute Q fever that caused frank encephalitis. We also review the literature on central nervous system disease attributable to C. burnetii.
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PMID:Encephalitis caused by Coxiella burnetii. 374 Aug 16

Acute infection of the central nervous system by the neurotropic JHM strain of mouse hepatitis virus (JHMV) induces nucleocapsid protein specific cytotoxic T lymphocytes (CTL) not found in the periphery (S. Stohlman, S. Kyuwa, J. Polo, D. Brady, M. Lai, and C. Bergmann, J. Virol. 67:7050-7059, 1993). Peripheral induction of CTL specific for the nucleocapsid protein of JHMV by vaccination with recombinant vaccinia viruses was unable to provide significant protection to a subsequent lethal virus challenge. By contrast, the transfer of nucleoprotein-specific CTL protected mice from a subsequent lethal challenge by reducing virus replication within the central nervous system, demonstrating the importance of the CTL response to this epitope in JHMV infection. Transfer of these CTL directly into the central nervous system was at least 10-fold more effective than peripheral transfer. Histological analysis indicated that the CTL reduced virus replication in ependymal cells, astrocytes, and microglia. Although the CTL were relatively ineffective at reducing virus replication in oligodendroglia, survivors showed minimal evidence of virus persistence within the central nervous system and no evidence of chronic ongoing demyelination.
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PMID:Mouse hepatitis virus-specific cytotoxic T lymphocytes protect from lethal infection without eliminating virus from the central nervous system. 781 31

Although hepatitis C virus (HCV) infection is very common, identification of patients during acute infection is rare. Consequently, little is known about the immune response during this critical stage of the disease. We analyzed the T lymphocyte response during and after acute resolving HCV infection in three persons, using interferon (IFN)-gamma enzyme-linked immunospot (ELISPOT) and human histocompatibility leukocyte antigen (HLA) peptide tetramer assays. Acute infection was associated with a broadly directed T helper and cytotoxic T lymphocyte (CTL) response, which persisted after resolution of clinical hepatitis and clearance of viremia. At the earliest time point studied, highly activated CTL populations were observed that temporarily failed to secrete IFN-gamma, a "stunned" phenotype, from which they recovered as viremia declined. In long-term HCV-seropositive persons, CTL responses were more common in persons who had cleared viremia compared with those with persistent viremia, although the frequencies of HCV-specific CTLs were lower than those found in persons during and after resolution of acute HCV infection. These studies demonstrate a strong and persistent CTL response in resolving acute HCV infection, and provide rationale to explore immune augmentation as a therapeutic intervention in chronic HCV infection.
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PMID:Analysis of successful immune responses in persons infected with hepatitis C virus. 1079 Apr 25

Acquired infection with hepatitis C virus (HCV) in hemodialysis patients has been described lately. In dialysis units in Italy and France, the prevalence and incidence of HCV are 20-60% and 1-2%, respectively. Most infected patients develop chronic hepatitis. The clinical presentation of acute HCV in hemodialysis patients is very mild and therefore the diagnosis is often made only by laboratory tests. Acute infection is usually followed by mild elevation of liver enzymes and the presence of HCV-RNA and anti-HCV in serum. We report a 48-year-old man on hemodialysis who developed acute hepatitis C. The diagnosis was made by finding mild elevation of liver enzymes and the presence of HCV-RNA in his serum. A few months later, he developed severe hepatitis which was followed by rapid deterioration in liver function. However, the virus was eradicated and liver function tests became normal. Surprisingly, serum anti-HCV antibodies were detected 5 months later.
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PMID:[Transmission of hepatitis C in hemodialysis patients--does one-time exposure result in chronic hepatitis?]. 1086 66

Hepatitis A remains an important cause of community-acquired hepatitis in the United States and in the world. In recent years, improvements in personal hygiene and environmental sanitation have led to declines in overall hepatitis A infection rates in developed countries, although sporadic outbreaks still occur with similar rates of hospitalization and loss of work. Therapy remains supportive and prevention holds the key to elimination of widespread infection. Acute infection can be prevented or attenuated with IG or with inactivated, highly immunogenic vaccines. Elderly persons and those with advanced liver disease are at higher risk of the consequences of acute HAV, and they represent target populations for immediate vaccination. Challenges for the future include strategies for broad-based population vaccination, including cost-effective approaches.
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PMID:Hepatitis A. 1098 12

Mice infected with neurotropic strains of mouse hepatitis virus (MHV) clear infectious virus; nevertheless, viral persistence in the central nervous system (CNS) is associated with ongoing primary demyelination. Acute infection induces a potent regional CD8+ T-cell response. The high prevalence of virus specific T cells correlates with ex vivo cytolytic activity, interferon-gamma (IFN-gamma) secretion and efficient reduction in virus. Viral clearance from most cell types is controlled by a perforin dependent mechanism. However, IFN-gamma is essential for controlling virus replication in oligodendrocytes. Furthermore, CD4+ T cells enhance CD8+ T-cell survival and effectiveness. Clearance of infectious virus is associated with a gradual decline of CNS T cells; nevertheless, activated T cells are retained within the CNS. The loss of cytolytic activity, but retention of IFN-gamma secretion during viral clearance suggests stringent regulation of CD8+ T-cell effector function, possibly as a means to minimize CNS damage. However, similar CD8+ T-cell responses to demyelinating and non demyelinating JHMV variants support the notion that CD8+ T cells do not contribute to the demyelinating process. Although T-cell retention is tightly linked to the presence of persisting virus, contributions to regulating the latent state are unknown. Studies in B-cell-deficient mice suggest that antibodies are required to prevent virus recrudescence. Although acute JHMV infection is thus primarily controlled by CD8+ T cells, both CD4+ T cells and B cells make significant contributions in maintaining the balance between viral replication and immune control, thus allowing host and pathogen survival.
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PMID:MHV infection of the CNS: mechanisms of immune-mediated control. 1127 May 93

Epstein-Barr virus (EBV) is a herpesvirus whose only reservoir host is the human. It is transmitted by oropharyngeal secretions. Primary EBV infection is usually asymptomatic, but sometimes it causes infectious mononucleosis with fever, lymphadenopathies, splenomegaly and pharyngitis. Acute infection is diagnosed by serology (heterophile or specific antibodies). Immunofluorescence and molecular biologic techniques may be used to demonstrate the presence of EBV in biopsy specimens. Mild and transient elevations of serum aminotransferases are common, thus liver biopsy is usually not necessary to confirm the diagnosis. Severe cholestasis is rare (5%). We describe a patient with cholestatic hepatitis and acute EBV infection with atypical lymphocytes and positive anti-VCA IgM. The patient had taken drugs (ibuprofen, paracetamol and valerian). The bad evolution of the patient, the history of exposure to drugs, and the few cases of cholestatic hepatitis due to EBV infection reported, led us to consider liver biopsy. Molecular biologic techniques confirmed the presence of EBV in liver tissue however histologic features did not exclude the toxic aetiology or the concomitant effect of drugs and EBV infection.
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PMID:[Epstein-Barr virus infection and acute cholestatic hepatitis]. 1713 11

Acute infection due to hepatitis C virus results in a chronic progression in 50-84% of cases. In the light of the risk of developing chronic disease and the response rate to treatment once the disease is established, it is very important to consider early treatment of acute hepatitis C before it progresses to the chronic form. The aim of this review is to evaluate the real efficacy and tolerance of Peg-interferon alpha-2b in monotherapy and in association with ribavirin in the treatment of patients affected by acute C hepatitis, to delineate the viral factors correlated with the sustained virological response and to consider when treatment should be started in relation to onset and what is the optimal duration of therapy. Also the pharmacodynamic and pharmacokinetic characteristics of PEG-IFN alpha-2b and ribavirin are reassessed. The analysis of literature demonstrates that Peg-interferon alpha-2b treatment is efficacious in terms of attaining sustained virological response (71-94% of cases). Treatment must be started within three months of onset and must be prolonged for three months. Only two studies have provided evidence the needed of a prolonged treatment for six months for genotype 1 infections. In all studies therapy has been generally well tolerated. Sustained virological response is independent of baseline viral load and of HCV genotypes in patients treated for six months, while in subjects treated for three months it seems to be dependent on HCV-genotype, with genotype 1 characterized by a less favourable outcome. Combination therapy with ribavirin does not seem to increase the response rate but could be proposed as a second choice to patients not responding to IFN monotherapy.
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PMID:PEG-interferon alpha-2b for acute hepatitis C: a review. 1769 45

Coxiella burnetii, the causative agent of Q fever, is a Gram negative coccobacillus. It resides and replicates in the host s monocytes and macrophages. The developmental cycle of C. burnetii includes macrocellular and microcellular forms and the formation of spore-like bodies. It undergoes a phase variation of outer cell surface antigens from virulent phase I to avirulent phase II after passaging in the yolk sac of embryonated chicken eggs or in cell cultures. C. burnetii belongs to the most resistant bacteria. The main reservoirs of C. burnetii are cattle, sheep and goats. Human Q fever usually results from inhalation of contaminated aerosols. Acute infection mostly takes the course of a flu-like disease, atypical pneumonia or hepatitis, the chronic form resembles endocarditis. Laboratory examinations are based on the presence of antibodies. The drugs of choice are broad-spectrum antibiotics.
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PMID:[Q fever]. 1770 1


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