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)

Epstein-Barr virus infection (EBV) was discovered 25 years ago in tumour cells from Burkitt's lymphoma. Extensive virological studies have relieved that EBV causes infectious mononucleosis and contributes to the pathogenesis of Burkitt's lymphoma and nasopharyngeal cancer. Atypical courses of the primary infection may induce meningoencephalitis or hepatitis and are attracting increasing attention. Antiviral treatment with acyclovir has been administered for 7 days, intravenously or orally, in the early stages of infectious mononucleosis, in 2 placebo controlled trials. An inhibition of oropharyngeal EBV replication was verified but minimal effects on clinical symptoms was observed. A combination of intravenous acyclovir and prednisolone treatment for 10 days was therefore tried in 15 patients with fulminant mononucleosis in a pilot study. A transient cessation of virus shedding was noticed in all patients, and a substantial clinical effect on pharyngeal symptoms and on fever was seen in 12/15 patients within 3 days. Treatment with chemotherapy or irradiation is recommended in EBV-associated B-cell lymphomas seen in immunosuppressed, transplanted, or human immunodeficiency virus-seropositive patients. No effect of acyclovir has been reported, but such therapy may be considered in the early stage when EBV induces a polyclonal B cell activation. Acyclovir treatment is effective in the EBV-genome positive hairy leukoplakia noticed in human immunodeficiency virus-seropositive patients. However, no effect of any antiviral therapy has been reported in the X-linked lymphoproliferative syndrome affecting in particular 2-7 year old boys. Prophylactic use of immunoglobulin or acyclovir has been suggested in susceptible children. These results indicate that the variety of clinical manifestations induced by EBV at least partly depend on the immune response elicited in the host and not of virus replication per se. Therefore, treatment of these various disorders cannot be generalized but must be based on the use of antiviral drugs combined with immunomodulatory agents.
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PMID:Clinical aspects on Epstein-Barr virus infection. 166 50

We have defined the clinical presentation and course of X-linked agammaglobulinemia (X-LA) by means of a multi-center retrospective survey of 96 patients. Infections were the most common presenting feature of patients with X-LA. The most frequent infections involved the upper respiratory tract (75%), lower respiratory tract (65%), gastrointestinal tract (35%), skin (28%), and central nervous system (16%). Clinical clues to the diagnosis of X-LA were the chronic or recurrent nature of infections, a family history of immunodeficiency, and infections at more than one anatomic location. Infections remained a significant problem after the diagnosis of X-LA was made and gamma-globulin prophylaxis had been instituted. One or more chronic infectious diseases occurred in 71% of patients. The respiratory tract was the most common site of disease, and the gastrointestinal tract was relatively spared. Patients died at a mean age of 17 years. The two major causes of death were chronic pulmonary disease with resultant cardiac failure, and disseminated viral infections which characteristically caused a dermatomyositis-like syndrome, hepatitis, pneumonitis, and meningoencephalitis.
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PMID:X-linked agammaglobulinemia: an analysis of 96 patients. 258 Nov 10

Enteroviral infections late in pregnancy are common, especially during periods of high prevalence of community infection. Most of these infections, however, are not associated with significant maternal or neonatal disease. Conversely, as many as 65 per cent of women who give birth to infants with proven enteroviral infection have symptomatic disease during the perinatal period. Maternal echovirus or coxsackievirus B infections are not associated with an increased risk of spontaneous abortions, but stillbirths late in pregnancy have been described. Although a slightly increased risk for congenital heart defects and urogenital anomalies has been reported for the offspring of women who seroconverted to the group B coxsackievirus during pregnancy, these data are highly tentative. Transmission of enteroviruses from mother to infant is relatively common (30-50 per cent) and may occur through contact with maternal secretions during vaginal delivery, blood, or upper respiratory tract secretions. Intrauterine transmission has been documented, but its frequency is unknown. Postnatal transmission from maternal or nonmaternal sources also occurs regularly. Neonatal disease may range from inapparent infection to overwhelming systemic illness and death. Common clinical syndromes associated with neonatal enteroviral infections are meningoencephalitis, pneumonia, myocarditis, and hepatitis. The severity and outcome of perinatally acquired enteroviral infection is influenced by several factors, including the virus strain involved, mode of transmission, and presence of passively acquired serotype-specific maternal antibody. Newborn nursery outbreaks of nonpolio enteroviral infections usually coincide with seasonal peaks of enteroviral disease in the community. These outbreaks have been due mostly to echovirus 11 or group B coxsackievirus serotypes 1 to 5 and are associated with attack rates of up to 50 per cent.
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PMID:Perinatal echovirus and group B coxsackievirus infections. 283 56

Cardiac involvement in patients with acquired immunodeficiency syndrome (AIDS) is being reported with increasing frequency, although the factors responsible for the cardiac abnormalities are rarely identified. We report a case of sudden and unexpected death of an infant with AIDS in whom histologic and virologic studies documented generalized infection with cytomegalovirus (CMV), including pancarditis, sialitis, nephritis, colitis, hepatitis, prostatitis, orchitis, myositis, pneumonitis, and meningoencephalitis. CMV was isolated from four of five tissues cultured. Lymphocytic infiltration in the region of the sinoatrial node could have been responsible for the development of a fatal cardiac arrhythmia, and the autopsy failed to reveal any other cause of death in this infant. Children infected with the human immunodeficiency virus (HIV) need to be closely monitored for cardiac complications bearing in mind that opportunistic infections in AIDS patients may cause cardiac involvement that is atypical or that is overshadowed by the primary manifestations of the infection.
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PMID:Unexpected death in an infant with AIDS: disseminated cytomegalovirus infection with pancarditis. 284 41

The organ tropism of MHV-A59, a murine coronavirus, was studied in 4-6 week-old C57BL/6 mice inoculated by different routes and with various amounts of virus. MHV-A59 caused hepatitis after intracerebral and intraperitoneal inoculation (two clearly artificial routes) and also after intranasal and intragastric inoculation (two routes more likely to mimic naturally acquired infection). For each route, the severity of hepatitis was dependent on the amount of virus inoculated. Significantly higher doses were needed to cause hepatitis by the intranasal or intragastric routes. We have shown previously that mice inoculated intracerebrally with MHV-A59 develop mild meningoencephalitis followed by chronic central nervous system (CNS) disease, characterized by primary demyelination (1). We extend these results here to show that acute CNS disease can be produced also by intranasal and intragastric inoculation, although much larger doses are needed as compared to intracerebral inoculation. Thus induction of demyelination, not only by the intracerebral route but also by the intranasal route, provides a useful model system to study virus-induced demyelination.
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PMID:The organ tropism of mouse hepatitis virus A59 in mice is dependent on dose and route of inoculation. 300 66

The in vivo infection of neonatal dogs by the microsporidian protozoan parasite, Encephalitozoon cuniculi, was studied. Microscopic examination of tissues from infected animals showed granulomatous nephritis, meningoencephalitis, hepatitis, and pneumonitis. A large component of the inflammatory infiltrate consisted of plasma cells and lymphocytes. In addition, hyperplasia of B-lymphocyte-dependent regions of lymph nodes and erythrophagocytosis were consistently seen in infected dogs. Infected dogs developed lymphocytosis, hypergammaglobulinemia, anti-encephalitozoon antibodies, and an antigen-specific blastogenic response to E. cuniculi spores. Lymphocyte blastogenic responses to the lectin phytohemagglutinin A (PHA) were depressed compared to controls. Dogs dying during the 2-month experimental trial were bacteremic. The findings of these experiments suggest that postnatal infection results in a demonstrable although seemingly ineffective immune and inflammatory response without detectable clinical disease.
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PMID:Experimental encephalitozoonosis in neonatal dogs. 310

The neuropathogenesis of Tyzzer's organism was comparatively studied in suckling and weanling mice after intranasal inoculation. In sucklings, suppurative rhinitis was produced in 24 hr postinoculation (p.i.) and organisms were detected in olfactory as well as supporting cells of the nasal mucosa. The lesions later developed to the lamina propria and propagation of organisms was seen within basal and glandular cells. On day 3 p.i., some organisms were found along with the olfactory nerve fibers and within neurons in the olfactory bulbs. Meningoencephalitis was produced with intraneuronal growth of bacteria on day 5 p.i. or later. On day 7 p.i., the brain lesions spread multifocally to the posterior parts and bacterial antigen in the nasal mucosa disappeared. In weanlings, infection was first established in the nasal mucosa and then some necrotized lesions were produced in the olfactory bulbs though much less in severity as compared to those of sucklings. Both suckling and weanling mice had necrotizing hepatitis while hemorrhagic enteritis was seen only in some sucklings.
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PMID:Neuropathogenesis of Tyzzer's organism in intranasally infected mice. 373 27

In the annuals of autopsy records in Japan, edited by the Japanese Society of Pathology and covering 20 years, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings. Of these, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found. The incidences of NSM and GCM were 0.11 and 0.007%, respectively. The annual incidence of NSM showed periodic fluctuations with in 5-year intervals and increased remarkably after 1974. Incidence of GCM showed a similar fluctuation but with a one to two year delay of peaks. The male to female ratio was 1.2: 1 and the age distribution had two peaked patterns for both sexes, though these peaks were scattered widely from neonate to elderly patients. The regional distribution of NSM showed a concentration in the middle portion of Honshu and its regional annual incidence had propagation waves from the central area to peripheral areas. The same tendency was observed in GCM cases. Hokkaido was characterized by a low incidence of NSM and no GCM. Complications of myocarditis included pancreatitis, pneumonitis, interstitial nephritis, meningoencephalitis, hepatitis, hepatic cirrhosis and a considerable incidence of malignancies. Antibiotics, antineoplastic agents, steroids and irradiation therapy were the main forms of treatment applied before or after the start of myocarditis.
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PMID:Twenty year autopsy statistics of myocarditis incidence in Japan. 382 May 37

In 1814, George Maton, first recognized that a mild illness characterized by rash, adenopathy, and little or no fever was a discrete entity. Henry Veale, in 1866, named the disease rubella. The illness attracted little attention until 1942, when Norman Gregg noticed that first-trimester maternal rubella caused serious birth defects. The full spectrum and impact of rubella embryopathy remained unclarified until rubella virus was isolated in tissue culture in 1962 by two independent groups: Parkman, Buescher, and Artenstein; and Neva and Weller. Using the new tools of the virus laboratory, many investigators concentrated on the consequences of a severe rubella epidemic in 1964, which affected approximately 1% of pregnancies. Newly recognized transient manifestations of congenital rubella infection (CRI) include neonatal thrombocytopenic purpura, hepatitis, bone lesions, and meningoencephalitis and late-emerging sequelae such as diabetes mellitus and progressive rubella panencephalitis added to the cataract, heart disease, mental retardation, and deafness previously defined as due to CRI. Sharp contrasts were documented between the patterns of virus excretion and immune response of postnatal vs. congenital rubella. Licensure and widespread distribution of attenuated rubella virus vaccines in 1969 have prevented epidemic rubella. Pockets of illness remain, even in the United States. Continued effort will be required to eliminate the rubella problem.
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PMID:The history and medical consequences of rubella. 389 Jan 5

Intracerebral inoculation of 4- to 6-week-old C57BL/6 mice with the A59 strain of mouse hepatitis virus (MHV), a murine coronavirus, produced biphasic disease. Acute hepatitis and mild meningoencephalitis were followed by subacute spastic paralysis with demyelinating lesions in the brain and spinal cord as determined by Epon-embedded toluidine-blue-stained sections and by electronmicroscopy. MHV-A59 was cultured by plaque assay from the blood, brain, spinal cord, and liver of infected mice during the acute phase, but not in the chronic stage. MHV-A59 antigen was detected by immunofluorescence (IF) until 3 months postinfection (PI). Serum anti-MHV-A59 antibodies were detected from 7 days to 5 months PI. The induction of demyelination by MHV-A59 provides a suitable system to study virus-induced demyelination further.
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PMID:Experimental demyelination produced by the A59 strain of mouse hepatitis virus. 632 31


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