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)

"Gigasept" is a highly efficient chemical disinfectant on the basis of succine dialdehyde and form aldehyde. The virucidal capacity was assayed in the suspension test procedure with different representative RNA and DNA viruses with and without an envelope, such as polio wild virus type I, coxsackie virus type B 3, adeno virus type 3, herpes virus type ) and vaccinia virus. Parameter for disinfectant activity was the virus inactivation kinetic, i. e. interdependence of titer reduction vs. disinfectant concentration and disinfectant contact time. A "minimal disinfection" was defined as a greater than or equal to 99.9% virus inactivation. A "disinfection per definitionem" must gain a titer reduction of greater than or equal to 10(3) ID 50 and absence of virus. According to these criteria all virus strains were inactivated by Gigasept regardless of absence or presence of serum, which was tested in a concentration of 40% calf serum. Disinfection per definitionem was achieved with Gigasept concentrations of 3% after 60 min. or 5% after 30 min. except for enteroviruses. This group of viruses has to be disinfected with a 10% solution for 4 hours or with a 5% solution overnight. Gigasept, on the basis of these results, can be classified as a highly effective virucidal disinfectant. As to the hepatitis virus group however, no data so far are available. An enterovirus - disinfection procedure is recommended in hepatitis risk areas, as long as test systems for hepatitis viruses are not developed.
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PMID:[Virucidal activity of the disinfectant "gigasept" against different enveloped and non-enveloped RNA-and DNA-viruses, pathogenic for men. I. Investigation in the suspension test (author's transl)]. 17 45

The course of infection of a pancreas-adapted isolate of coxsackievirus B4 was followed over a 10 month period in a murine model. Following intraperitoneal inoculation a typical acute infection was seen in nine of 10 inbred mouse strains. Virus rapidly infected the exocrine pancreas, titres peaking 3 to 4 days post-infection (p.i.). Lesions were almost exclusively confined to pancreatic acinar cells and varied in severity among the inbred strains. Virus shed into the blood-stream was not cell-associated. Evidence of persistent infection was found in nine mouse strains and infective virus was recovered from the pancreas of seven strains for up to 10 months p.i. Approximately 28% of pancreases examined beyond the acute phase showed focal inflammation and 22% showed focal necrosis (cell death). Virus was occasionally recovered from other organs (heart, liver and spleen), but lesions were rarely seen. Virus-specific antigen was localized to small groups of pancreatic acinar cells using an indirect immunogold silver staining technique. These observations suggested that the virus persists in pancreatic tissues because it seems unlikely that virus disseminated from distant sites would cause such localized infection. In three of these strains, the course of infection may have been influenced by superinfection with mouse hepatitis virus.
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PMID:Coxsackievirus B4 infection of the mouse pancreas: acute and persistent infection. 160 60

A random primed lambda gt11-cDNA library was constructed from donors plasma presumably infected by blood-borne non-A, non-B hepatitis (hepatitis C:HC) agent and immunoscreened with serum pooled from patients with acute or chronic HC. Twelve lambda gt11-cDNA clones encoding antigens associated with HC infection in Japan as well as in the USA were isolated. Of these one clone consisting of 114 nucleotides and showing a discrete band on an immunoblot analysis, was extensively studied. The clone is not derived from the host DNA encoding one polypeptide specific and highly sensitive for serum from patients with HC and has no homology to the nucleotide sequences of known human viruses including hepatitis A,B and D viruses, Ebstein-Barr virus, coxsackievirus, immunodeficiency virus type 1 or Japanese encephalitis virus. These results suggest that this clone is derived from the genome of HC agent.
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PMID:A cDNA clone encoding a peptide highly specific for hepatitis C infection. 169 49

A random primed lambda gt11-cDNA library was constructed from donors plasma presumably infected by blood-borne non-A, non-B hepatitis (hepatitis C:HC) agent and immunoscreened with serum pooled from patients with acute or chronic HC. Twelve lambda gt11-cDNA clones were isolated that was shown to encode antigens associated specifically with HC infection in Japan as well as in USA. Of these two, as well as another clone which is specific only to Japanese HC infection, have unique nucleotide sequences and were extensively studied. They are not derived from host DNA and have no homology to the sequences of known human viruses including hepatitis A, B and D viruses, Ebstein-Barr virus, coxsackievirus, immunodeficiency virus type 1 or Japanese encephalitis virus. These results suggest that they are derived from the genome of HC agent(s). In addition, of these, one clone seems to encode epitopes derived from both the core and the surface polypeptides of the agent.
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PMID:Cloning of hepatitis C virus genomes and their properties. 169 32

Sensitive and specific methods are needed to detect hepatitis A virus (HAV) and other human enteroviruses in environmental samples such as drinking water and foods. Clones of cDNA encoding the 5'-most 1 kb of the HAV and coxsackievirus B3 (CB3) genomes were subcloned into T7/SP6 RNA transcription vectors. In vitro transcribed RNA from the T7 promoter detected their respective HAV or CB3 genomic RNA. Conversely, SP6 transcripts detected viral negative-stranded RNA but not the genome. When both ssRNA probes were tested at high temperature (65 degrees C), they did not hybridize with intracellular RNAs from 6 primate cell cultures used for isolation of HAV and other enteroviruses. The HAV probe did not hybridize with 13 different enteroviruses but detected as little as 500-1000 infectious units of the 7 strains of HAV tested. Conversely, the CB3 probe showed strong homology with all 13 enteroviruses tested but not HAV. The probes were used to detect HAV and other enteroviruses in water samples after virus amplification in cell culture. HAV was detected in water samples obtained during a waterborne hepatitis outbreak using the ssRNA probe. These samples were negative for HAV by direct solid phase radioimmunoassay and were not positive by immunoassays of inoculated cell cultures until several weeks of propagation. The CB3 ssRNA probe detected enteroviruses in samples of surface water and drinking water that were negative for cytopathic effects in inoculated cell cultures.
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PMID:Detection of hepatitis A virus and other enteroviruses in water by ssRNA probes. 184 14

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

We describe a severe multisystem Coxsackie virus type B3 infection in a previously healthy 14-year-old girl who presented with a mononucleosis-like syndrome (MS). Initial observations included a prominent cervical lymphadenopathy, exudative pharyngitis and leucocytosis with atypical lymphocytosis. At the end of the 2nd week of illness the patient developed meningoencephalomyelitis and haemolytic anaemia. Subclinical myocarditis was also recorded. Prolonged hepatitis recrudescing at the time of recovery coincided with serological evidence of a reactivated Epstein-Barr virus infection. The diagnosis was based on a significant rise in serum antibody titres against Coxsackie virus type B3, using the neutralization test. Intrathecal synthesis of antibodies to Coxsackie virus type B3 was also demonstrated. Generalized Coxsackie virus infections in adolescence are rare and an MS has not, to our knowledge, been associated with Coxsackie virus type B3 infection.
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PMID:Mononucleosis-like syndrome associated with a multisystem Coxsackie virus type B3 infection in adolescence. 284 Feb 91

Epidemiologic studies suggest an association between insulin dependent diabetes mellitus and viral infections. Several candidates like cytomegalovirus, Coxsackie virus and hepatitis virus have a selective tropism for beta cells. Progress in the understanding of the pathogenic importance of such viruses has been facilitated by animal models with virus induced diabetes and infections of human pancreatic beta cells maintained in culture. Immunological studies of type I diabetes after viral infections suggest that virus may trigger pancreatic autoimmunity. Molecular mimicry between viral and tissue antigens may represent a possible mechanism. Loss of immune tolerance toward beta cells would only appear in genetically predisposed individuals. The better understanding of the pathogenesis of type I diabetes mellitus brings out new approaches to treatment.
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PMID:[Virus and insulin-dependent diabetes mellitus. Etiopathogenic perspectives]. 327 88

During an outbreak of infectious hepatitis at a housing development, Coxsackie A10 virus was recovered from the stools of 45 different contacts and from the blood of four others. Caution should be exercised in attributing an etiological role to any given isolate of a Group A Coxsackie virus in view of the widespread distribution of these organisms. Nevertheless, the recovery of Coxsackie A10 viruses from the blood and stools of contacts with hepatitis cases appears to warrant record.
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PMID:Coxsackie A10 virus infection among infectious hepatitis contacts. 582 98

Studies of data from ten cases of infantile acrodermatitis and from eight cases reported in the North American literature disclose distinctive papular dermatosis of the face and extremities, often related to virus infection. None of our eight patients who were tested had evidence of hepatitis B infections, although transaminase values were elevated in two. All five patients who were tested had lymphocytosis. Six patients had antecedent upper respiratory tract symptoms. Data from our cases and from the other previously reported cases indicate that the eruption is a virus-related response. Although the hepatitis virus has been the most frequently encountered causative agent to date, other viruses, including Epstein-Barr virus, coxsackievirus, and parainfluenza virus, may produce a similar cutaneous response.
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PMID:Gianotti-Crosti syndrome. A review of ten cases not associated with hepatitis B. 632 7


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