Disease relevance of Hepatitis A

• A case was defined by the presence of typical signs and symptoms, a diagnostic increase in IgM antibody to hepatitis A, and a serum concentration of alanine aminotransferase at least twice the upper limit of normal [1].
• Among the various viral and liver diseases studied RIF appeared to be specific for hepatitis A and B viral infections [2].
• Thus, percentage survival for the acetaminophen-overdose cases was 52.9%, for hepatitis A 66.7%, for hepatitis B 38.9%, for presumed non-A, non-B hepatitis 20%, and for halothane or drug reaction 12.5% [3].
• Patients with parvovirus B19 infection had significantly lower bilirubin concentrations than age-matched patients with FH due to hepatitis A (nine) or other causes (nine) (poisoning with amanita excluded) [4].
• Acute and convalescent sera from 368 patients drawn from a 3-year survey of viral hepatitis in West London were tested for radioimmunoassay for evidence of recent infection with hepatitis A or B and, if neither was found, antibody to Epstein-Barr (EB) virus and cytomegalovirus [5].

High impact information on Hepatitis A

• Steroid therapy in severe viral hepatitis. A double-blind, randomized trial of methyl-prednisolone versus placebo [6].
• TIM-1 is genetically linked to asthma and is a receptor for hepatitis A virus, but the endogenous ligand of TIM-1 is not known [7].
• The human homolog of TIM-1 is the hepatitis A virus (HAV) receptor, which may explain the inverse relationship between HAV infection and the development of atopy [8].
• Infectious hepatitis C virus pseudo-particles containing functional E1-E2 envelope protein complexes [9].
• We tested the hypotheses that the risk of asthma is reduced by intestinal parasites or hepatitis A infection, and increased by exposure to dust-mite allergen or organophosphorus insecticides in urban and rural areas of Jimma, Ethiopia [10].

Chemical compound and disease context of Hepatitis A

• Hepatitis A in three patients taking sodium valproate [11].
• During the follow-up period, 35 (74%) of 47 patients with intrahepatic disease showed a reduction of LP-X; of the remaining 12 patients 4 had mitochondrial antibody-positive primary biliary cirrhosis, and 6 had severe cholestasis associated with acute infectious hepatitis and high aspartate transaminase levels [12].
• Isoniazid-rifampin fulminant hepatitis. A possible consequence of the enhancement of isoniazid hepatotoxicity by enzyme induction [13].
• Identification of a surface glycoprotein on African green monkey kidney cells as a receptor for hepatitis A virus [14].
• We conclude that hepatitis A virus rarely if every spreads by parenteral mechanisms, that there is no epidemiologic evidence confirming the existence of chronic hepatitis A viremic carrier states, and that hemodialysis does not play a significant role in the spread of type A hepatitis [15].
• Revaccination of nonresponders to the standard hepatitis B vaccine regimen with a double dose of the combined hepatitis A and B vaccine was highly effective [16].

Biological context of Hepatitis A

• A hepatitis A virus deletion mutant which lacks the first pyrimidine-rich tract of the 5' nontranslated RNA remains virulent in primates after direct intrahepatic nucleic acid transfection [17].
• We have examined the requirement of the cellular protein poly(rC) binding protein 2 (PCBP2) for hepatitis A virus (HAV) RNA translation [18].
• Serial stools and sera from 13 patients with hepatitis A were collected during an epidemic in 1978 in a rural village near Hangzhou, China, and were studied to determine the patterns of shedding of hepatitis A antigen (HAAg) and of antibody response in some cases [19].
• Inhibitory effects of atropine, protamine, and their combination on hepatitis A virus replication in PLC/PRF/5 cells [20].
• A solid-phase antibody capture hemadsorption (SPACH) assay was developed to detect hepatitis A virus (HAV)-specific immunoglobulin M (IgM) antibodies in sera from humans recently infected with hepatitis [21].

Anatomical context of Hepatitis A

• In these 2 subjects, specific helper T cells and antibodies to the asialoglycoprotein receptor persisted and increased after acute hepatitis A, and autoimmune CAH type 1 developed within 5 months [22].
• Scattered microscopic polymorphonuclear leukocyte accumulations were seen that contained extracellular alpha 1-antitrypsin material, but there was neither histological nor serological evidence of mouse infectious hepatitis [23].
• These results imply that hepatitis A virus infection may be controlled by lymphocyte responses in the liver, i.e., by lymphocyte-mediated lysis of the hepatitis A virus-infected cells, and by the production of high titers of IFN-alpha by lymphocytes exposed to hepatitis A virus-infected cells [24].
• Cell culture-adapted variants of hepatitis A virus (HAV) in which the first pyrimidine-rich tract (pY1; nucleotides 99 to 138) of the 5' nontranslated region has been deleted (delta 96-137 or delta 96-139) replicate as well as parental virus in cultured cells (D.R. Shaffer, E.A. Brown, and S.M. Lemon, J. Virol. 68:5568-5578, 1994) [17].
• Acute- and convalescent-phase sera, and cerebrospinal fluid, when applicable, underwent diagnostic evaluation for infections with Dengue virus (DENV), Japanese encephalitis virus (JEV), and Hepatitis A, B, C, and E viruses [25].

Gene context of Hepatitis A

• Hepatitis A virus suppresses RIG-I-mediated IRF-3 activation to block induction of beta interferon [26].
• In patients with infectious hepatitis or with malignant disease of the liver t-PA was normal whereas u-PA and PAI-1 were increased [27].
• Plasminogen activators and plasminogen activator inhibitors in liver deficiencies caused by chronic alcoholism or infectious hepatitis [27].
• Human KIM-1 exhibits homology to a monkey gene, hepatitis A virus cell receptor 1 (HAVcr-1), which was identified recently as a receptor for the hepatitis A virus [28].
• The Cys-rich region of hepatitis A virus cellular receptor 1 is required for binding of hepatitis A virus and protective monoclonal antibody 190/4 [29].

Analytical, diagnostic and therapeutic context of Hepatitis A

• Immunoglobulin M, G, and A concentrations were determined by radial immunodiffusion in sera collected from 117 patients with acute hepatitis A, hepatitis B, or non-A, non-B hepatitis [30].
• A functional polymorphism in the IL-10 promoter influences the response after vaccination with HBsAg and hepatitis A [31].
• In situ hybridization with oligonucleotide probes has been used to localise hepatitis A virus RNA genomic sequences in formalin-fixed and routinely processed human liver biopsies from three patients [32].
• This filtration process allows the elimination of small particles, such as non-enveloped viruses (i.e., hepatitis A and parvovirus B19) [33].
• Determination of immunoglobulin M antibodies against hepatitis B core antigen and hepatitis A virus by reorienting sucrose gradient high-speed centrifugation for diagnosis of acute viral-hepatitis [34].

References