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)

In the period of reduced incidence of viral hepatitis in Tajikistan, January-December, 1990, 1562 patients with acute viral hepatitis (AVH) were examined in the first days of the jaundice phase (928 children under 14 years and 634 adults) in Dushanbe. Markers of hepatitis A, B, and D (HBsAg, anti-HA IgM, anti-HBc IgM, anti-delta IgM) were determined by enzyme immunoassay. Hepatitis A occurred in 25.8% of the patients with AVH, mostly children of 1-6 years, HB in 22.8%, HD co- and superinfection) in 9.2%. In 42.1% of the patients who had no HA, HB, or HD markers in the blood, non-A, non-B hepatitis (mostly hepatitis E) was diagnosed, mainly in the age groups of 30-39 years (70.7%) and 15-29 years (59.2%). Thus, in Tajikistan hepatitis E occurs not only during outbreaks of this infection but also sporadically.
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PMID:[The etiological structure of acute viral hepatitis in Tadzhikistan in a period of decreased morbidity]. 183 51

A sample of patient's faeces containing virus-like particles (VLP) of 27-34 nm was obtained during an outbreak of hepatitis E in the Kirghiz SSR. The identity of the VLP to hepatitis E virus and etiological association with the disease were demonstrated by immune electron microscopy and infection of Macaca fascicularis monkeys. This isolate of hepatitis E virus is able to induce experimental infection in domestic piglets which was very similar to experimental hepatitis E in primates when infected orally, intravenously and by the combined routes. The clinical manifestations included acute biochemical and histological hepatitis, excretion of hepatitis E virus in faeces, icteric sclerae and skin, hepatitis virus presence in the material from mesenteric lymph nodes. Immunosuppression aggravated hepatitis E infection in piglets. Piglet-to-piglet transmission of hepatitis E virus was demonstrated. During passages of the virus in piglets a shortening of the incubation period and the absence of jaundice was observed.
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PMID:[Experimental hepatitis E infection in piglets]. 189 76

We have recently described the cloning of a portion of the hepatitis E virus (HEV) and confirmed its etiologic association with enterically transmitted (waterborne, epidemic) non-A, non-B hepatitis. The virus consists of a single-stranded, positive-sense RNA genome of approximately 7.5 kb, with a polyadenylated 3' end. We now report on the cloning and nucleotide sequencing of an overlapping, contiguous set of cDNA clones representing the entire genome of the HEV Burma strain [HEV(B)]. The largest open reading frame extends approximately 5 kb from the 5' end and contains the RNA-directed RNA polymerase and nucleoside triphosphate binding motifs. The second major open reading frame (ORF2) begins 37 bp downstream of the first and extends approximately 2 kb to the termination codon present 65 bp from the 3' terminal stretch of poly(A) residues. ORF2 contains a consensus signal peptide sequence at its amino terminus and a capsid-like region with a high content of basic amino acids similar to that seen with other virus capsid proteins. A third open reading frame partially overlaps the first and second and encompasses only 369 bp. In addition to the 7.5-kb full-length genomic transcript, two subgenomic polyadenylated messages of approximately 3.7 and 2.0 kb were detected in infected liver using a probe from the 3' third of the genome. The genomic organization of the virus is consistent with the 5' end encoding nonstructural and the 3' end encoding the viral structural gene(s). The expression strategy of the virus involves the use of three different open reading frames and at least three different transcripts. HEV was previously determined to be a nonenveloped particle with a diameter of 27-34 nm. These findings on the genetic organization and expression strategy of HEV suggest that it is the prototype human pathogen for a new class of RNA virus or perhaps a separate genus within the Caliciviridae family.
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PMID:Hepatitis E virus (HEV): molecular cloning and sequencing of the full-length viral genome. 192 70

An outbreak of acute hepatitis E virus (HEV) infection occurred from October 1988 to March 1989 in military camps in northern Ethiopia. The epidemic was waterborne and entirely confined to military men, of whom 423 hospitalized, icteric patients were studied. The clinical course was mild and short, without any fulminant hepatitis or death. All sera tested for anti-HAV-IgM were negative and among 54 (13%) patients who were positive for HBsAg, 7 (2%) were positive for anti-HBc IgM. On the other hand, 28 of 30 (93%) patients had antibodies against hepatitis E virus (anti-HEV) in contrast to 1 of 29 (3%) asymptomatic controls (P less than .01). The need for an easily available, inexpensive serologic test for HEV infection, protection of water supplies from fecal contamination, adequate chlorination and/or boiling of drinking water, and health education about personal and environmental hygiene, especially in communities at high risk, is emphasized.
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PMID:Outbreak of acute hepatitis E virus infection among military personnel in northern Ethiopia. 194 Aug 76

Epidemiological studies on SRSVs, human calicivirus and astroviruses have been limited by the problems of establishing them in cell culture and the inability to transmit them to animals or to use strains from animals as a source of antigen for diagnostic tests. The use of EM and the subsequent development of RIAs and EIAs in a few research centres has shown that they are a cause of outbreaks and sporadic cases of diarrhoea and vomiting. SRSVs have increasingly been recognized as a major cause of outbreaks of gastroenteritis in the community and in hospital wards. The symptoms of illness are generally mild and of short duration and patients seldom require medical attention. However, because of the high attack rates and large numbers of persons of all age groups involved, there is often considerable economic loss and disruption of services. Evidence is accumulating that polluted water, molluscan shellfish, and contaminated cold foods are major sources of infection. Recently a SRSV has been shown to be the cause of epidemics and sporadic cases of waterborne enterically transmitted non-A, non-B hepatitis (hepatitis E virus) which have occurred in the USSR, India, Mexico and Africa. Astroviruses and human caliciviruses are occasional causes of outbreaks of vomiting and diarrhoea in infants and the elderly which can necessitate the closure of hospital wards and cause considerable disruption. Symptoms are generally mild and of short duration and therefore the majority of cases are unlikely to be investigated by laboratories. Diagnosis of infections is at present limited to the few laboratories that have developed their own assays or have access to electronmicroscopy facilities.
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PMID:Human, small round structured viruses, caliciviruses and astroviruses. 196 28

Hepatitis Delta virus (HDV) is an incomplete virus dependent on the hepatitis B virus (HBV) for its replication. Serologic studies have shown that HDV is found all over the world. However, the prevalence is not simply a function of the prevalence of HBV, but HDV has an epidemiology of its own with major geographic differences as exemplified below. A high rate with as many as 60-80% anti-HDV positives among chronic HBsAg-carriers has been found in the northern part of South America, Central Africa and Asiatic Russia. In Europe, USA and Australia the prevalences of anti-delta among chronic HBV carriers in the general population are low. It is high, however, in special risk groups such as drug addicts. In the Far-East a very low frequency of anti-HDV is found. There are two different types of non-A, non-B hepatitis, transmitted either enterically or parenterally. The different agents are now partly characterized. The agent causing enterically transmitted disease has characteristics comparable with calici virus. The designation hepatitis E virus has been proposed. Epidemics of hepatitis caused by this agent has been found in three continents. The outbreaks have been associated with fecal contamination of drinking water. The agent causing parenterally transmitted non-A, non-B hepatitis has been reported to be partly defined by molecular hybridization techniques and is probably related to flavi virus. The name hepatitis C virus has been proposed. Parenterally transmitted non-A, non-B is predominantly seen in recipients of blood or blood products and among drug addicts.
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PMID:Epidemiology of hepatitis delta virus and non-A, non-B hepatitis. 196 20

Hepatitis B is the target disease whenever one considers the scientific basis for the procedures to prevent cross contamination between patients. Thus, hepatitis B is the infectious disease that health care workers must review (occasionally) to remain current in the recognition and prevention of infection. This article provides a review and the latest information on non-A, non-B hepatitis (hepatitis C and hepatitis E) and hepatitis B vaccines.
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PMID:Hepatitis B. Current status in dentistry. 203 75

Major epidemic outbreaks of viral hepatitis in underdeveloped countries result from a type of non-A, non-B hepatitis distinct from the parenterally transmitted form. The viral agent responsible for this form of epidemic, or enterically transmitted non-A, non-B hepatitis (ET-NANBH), has been serially transmitted in cynomolgus macaques (cynos) and has resulted in typical elevation in liver enzymes and the detection of characteristic virus-like particles (VLPs) in both feces and bile. Infectious bile was used for the construction of recombinant complementary DNA libraries. One clone, ET1.1, was exogenous to uninfected human and cyno genomic liver DNA, as well as to genomic DNA from infected cyno liver. ET1.1 did however, hybridize to an approximately 7.6-kilobase RNA species present only in infected cyno liver. The translated nucleic acid sequence of a portion of ET1.1 had a consensus amino acid motif consistent with an RNA-directed RNA polymerase; this enzyme is present in all positive strand RNA viruses. Furthermore, ET1.1 specifically identified similar sequences in complementary DNA prepared from infected human fecal samples collected from five geographically distinct ET-NANBH outbreaks. Therefore, ET1.1 represents a portion of the genome of the principal viral agent, to be named hepatitis E virus, which is responsible for epidemic outbreaks of ET-NANBH.
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PMID:Isolation of a cDNA from the virus responsible for enterically transmitted non-A, non-B hepatitis. 210 74

Two distinct forms of non A non B viral hepatitis are now distinguished: (a) parenterally transmitted non A non B hepatitis, mainly due to hepatitis C virus, (b) enterically transmitted non A non B hepatitis, mainly due to hepatitis E virus. Hepatitis C virus is an enveloped, 50 to 60 nm in diameter, single stranded RNA virus. Its transmission is essentially parenteral and resembles that of hepatitis B virus. Individuals at risk are those in contact with blood products. Sexual transmission is uncommon. C virus hepatitis is characterized by a frequent course to chronic hepatitis, cirrhosis and hepatocellular carcinoma. Fulminant hepatitis is rare. Chronic forms are associated with the presence of anti-HCV antibodies in the serum. These antibodies are rarely present in the acute stage of the disease. Hepatitis E virus is a non-enveloped, 30 nm in diameter, single stranded RNA virus. Its transmission is faecal-oral, thus similar to that of hepatitis A virus. The disease is almost exclusively encountered in developing countries. It is not observed in France, apart from imported cases. Like A virus hepatitis, chronicity never occurs. Fulminant hepatitis is possible in pregnant women in the third trimester of pregnancy. There is no routine serological test. Development of vaccines against these two viruses can be expected.
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PMID:[Non-A non-B acute hepatitis]. 211 1

In the United Kingdom and United States of America, fulminant viral hepatitis is due mainly to sporadic (non-parenteral) non-A, non-B hepatitis and hepatitis B whereas that caused by hepatitis A virus is very uncommon and by the herpes viruses remains rare. Recent advances in fulminant non-A, non-B hepatitis have come with the identification and cloning of a virus (27-34 nm) in the enteral variety (hepatitis E) which is prevalent in the Indian sub-continent, North Africa and elsewhere, especially in pregnant women. Virus-like particles (50-70 nm) with ultrastructural features similar to the togaviridae and flaviviridae have been identified in some patients with fulminant non-A, non-B hepatitis in the United Kingdom. The relation to hepatitis C virus, recently identified as a major cause of chronic post-transfusion (parenteral) non-A, non-B hepatitis, awaits serological analysis. The recent demonstration that persistence of active viral replication can occur in some cases of fulminant hepatitis types A and B using monoclonal antibody and molecular biology techniques challenges the classical views on the pathogenesis of these varieties of fulminant viral hepatitis.
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PMID:Fulminant viral hepatitis. 211 14


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