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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis C virus (HCV) is a recently described causative agent of the great majority of post-transfusion non A-non B hepatitis and is classified within the Flaviviridae family. Due to a high prevalence of anti-HCV and other flaviviruses circulating in Brazil, such as dengue and yellow fever, we investigated the possibility of serological cross-reactivity between these viruses. Different panels of human sera positive for dengue type 1 (9 cases) and type 2 (7 cases) from 6 patients naturally infected with yellow fever and from 94 adults vaccinated against the 17D strain of yellow fever were tested against HCV antigens used in diagnostic assays. Two enzyme immunoassay systems were tested: one, an in-house test using recombinant antigens from core, NS3 and NS5 regions of the HCV genome (Research Foundation for Microbial Disease of Osaka University, Japan); and another, using synthetic peptides representing immunodominant epitopes of structural core and non-structural NS4 and NS5 HCV regions (INNOTEST HCV Ab, Innogenetics, Belgium). A line immunoassay (INNO-LIA HCV Ab, Innogenetics, Belgium) was used as a confirmatory test. In this, HCV antigens are coated as discrete lines on a nylon strip with plastic backing. Besides 4 control lines on each strip, a total of 6 HCV lines are present: line A consists of several NS4 epitopes, line B consists of several NS5 epitopes and lines C-F contain several core epitopes. This test not only confirms but differentiates antibodies to hepatitis C virus. No positive results were detected with these tests, indicating that hepatitis C infection can be evaluated by current assays in regions where flaviviruses are endemic.
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PMID:Human antibodies to dengue and yellow fever do not react in diagnostic assays for hepatitis C virus. 128 68

The impact of dengue on liver function was studied by biochemical tests on 125 male and 145 female patients diagnosed with this disease during an outbreak that extended from November 1987 to December 1988. Abnormal levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, alkaline phosphatase, and gamma-glutamyl transpeptidase (G-GT) were observed in 93.3%, 82.2%, 7.2%, 16.3% and 83.0% of the patients, respectively. The elevation of transaminases was mild to moderate in most cases, but was 10-fold greater than the normal upper limit for AST and ALT in 11.1% and 7.4% of the patients, respectively. Initially, the level of AST was greater than that of ALT, increasing to maximum levels nine days after the onset of symptoms, then decreasing to normal levels within two weeks. Results of the biochemical tests did not differ significantly between the cases with and without hepatitis B or hepatitis C virus infection, but significantly higher elevations of AST, ALT, and G-GT were observed in patients with episodes of bleeding. Liver biopsies of two patients showed features of lobular hepatitis. Of the five fatal cases, three died of hepatic failure. It is concluded that dengue fever may cause hepatic injury and transaminase elevation similar to that in patients with conventional viral hepatitis. In epidemic or endemic areas, dengue fever infection should be considered in the differential diagnosis of hepatitis.
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PMID:Liver biochemical tests and dengue fever. 135 50

Haematological syndromes attributed to viruses demonstrate geographical variations in incidence and great dependence on host factors. Severe haematological disease is the exception rather than the rule in dengue virus infection, and probably depends at least in part on the host immune response to the virus. The increased incidence of hepatitis-associated aplasia in east Asia may reflect distribution of an infectious agent, an environmental toxin, or genetic predisposition, but probably represents some combination of these factors. Agents with apparently universal distribution, such as parvovirus B19 and Epstein-Barr virus, are associated with bone marrow failure only in a very narrow range of hosts. These examples teach us that viral causes cannot automatically be excluded from the differential diagnosis of syndromes whose occurrence is rare or apparently sporadic. Further investigation of these syndromes should include more detailed characterization of host factors, particularly immunological characteristics, and possible infectious and toxic cofactors which are associated with morbidity.
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PMID:Viruses and the blood. 151 Nov 77

Many agents are associated with bone marrow failure, including toxins, inherited metabolic defects, ionizing radiation, and viral infection. In most cases, the etiologic agent is unknown. Many of these unclassified cases have symptomatic, immunologic, or epidemiologic similarities to viral infections. Viruses from different taxonomic families have been implicated in bone marrow failure syndromes, and they appear to cause hematosuppression by a variety of mechanisms. Some of the viruses involved in relatively well characterized suppressive interactions will be reviewed, including parovovirus B19, dengue, hepatitis viruses, Epstein-Barr virus, cytomegalovirus and the human immunodeficiency virus.
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PMID:Viruses and bone marrow failure. 165 29

Hepatitis C virus (HCV) is an important human pathogen that is associated with transfusion-related non-A, non-B hepatitis. Recently, HCV cDNA was cloned and the nucleotide sequence of approximately three-quarters of the virus genome was determined. A region of the predicted polyprotein sequence was found to share similarity with a nonstructural protein encoded by dengue virus, a member of the flavivirus family. We report here that HCV shares an even greater degree of protein sequence similarity with members of the pestivirus group (i.e., bovine viral diarrhea virus and hog cholera virus), which are thought to be distantly related to the flaviviruses. In addition, we find that HCV shares significant protein sequence similarity with the polyproteins encoded by members of the picornavirus-like and alphavirus-like plant virus supergroups. These data suggest that HCV may be evolutionarily related to both plant and animal viruses.
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PMID:Hepatitis C virus shares amino acid sequence similarity with pestiviruses and flaviviruses as well as members of two plant virus supergroups. 215 59

A pilot epidemiologic study of all cases of Reye and Reye-like syndromes was undertaken at 8 representative major hospitals in Peninsular Malaya from January 1st to December 31st 1986. The cases were classified as definitive Reye's syndrome, clinical Reye's syndrome and encephalo-hepatopathies. Less than 50% of cases reviewed fulfilled the National Center for Disease Control criteria for clinical Reye's syndrome. Causes of Reye-like syndromes/encephalo-hepatopathies included fulminant hepatitis, Japanese B encephalitis, dengue, septicaemia, and complex febrile fits. It was not possible to differentiate clinical Reye's syndrome from the other encephalo-hepatopathies by either the clinical features (except for jaundice) or biochemical parameters. Liver biopsy is necessary for a definitive diagnosis of Reye's syndrome in Malaysia, because of the high prevalence of Reye-like diseases. The mortality rate in the 2 groups of patients is similar. Ingestion of salicylates was not found to be significantly associated with Reye and Reye-like syndromes in this study.
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PMID:Reye and Reye-like syndromes: results of a pilot study in Peninsular Malaya, 1986. 228 20

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

To determine the extent of hantavirus infection in Singapore, serological studies using the indirect immunofluorescent antibody (IFA) test were conducted on commensal rodents and on human patients in 4 diagnostic groups. Virus isolation using a Vero E6 cell line was performed on hantaviral antigen-positive rodent lung tissue. Of 142 rodents and 3 insectivores studied, 37 (26%) were seropositive for IFA. Rattus norvegicus was the predominant species captured, with the highest species-specific seropositive rate of 32% (36 of 113). A hantavirus strain, R36, was isolated from one R. norvegicus. Seropositive rates for human patients were: 8% respectively for dengue haemorrhagic fever suspects and for non-A non-B hepatitis patients, 3% for leptospirosis suspects and 2% for acute nephritis patients. 2 patients had marked liver dysfunction but mild renal involvement. This hepatitis-like manifestation appears to be a clinical variant of hantavirus infection.
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PMID:Hantavirus infections in humans and commensal rodents in Singapore. 257 93

Four recent cases of dengue fever with severe, unusual clinical manifestations are described. Two of these cases had features of fulminant hepatitis and encephalopathy; one of these cases was fatal. The two remaining cases showed hepatitis with renal impairment. The significance and importance of these unusual manifestations of dengue disease are discussed.
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PMID:Unusual clinical manifestations of dengue virus infection. 323 69

Dengue hemorrhagic fever/dengue shock syndrome is a serious manifestation of dengue fever, which is observed predominantly in the tropical regions of the West Pacific and in Southeast Asia and is associated with secondary infections, mainly in children under age 15. A concomitant microangiopathic coagulopathy has been described; moreover, encephalopathy and even Reye's syndrome have been rarely reported. This report describes a 51-year-old man with secondary dengue infection who presented with clinical evidence of severe hepatitis, encephalopathy, cranial nerve palsy, and microangiopathic coagulopathy and who had a favorable outcome. A careful surveillance for the occurrence of secondary dengue in the Western Hemisphere is proposed, and dengue is suggested as a diagnostic possibility in obscure febrile illnesses presenting as either hepatitis, encephalopathy, or coagulopathy in places in which the mosquito vector, Aedes aegypti, is present.
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PMID:Dengue and hepatic failure. 406 82


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