Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0021400 (influenza)
 57,666 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The structural integrity of epithelial cells of the lateral choroid plexus tissues from the ferret model for Reye's syndrome was examined by transmission electron microscopy after the animals were inoculated intranasally with influenza B, were administered aspirin, and/or were fed an arginine deficient diet singly and in combination. No cellular alteration in the choroidal epithelium was caused by influenza B nor by aspirin, however, the synthetic diet produced random intercellular edema. The structural integrity of choroidal epithelial cells appeared intact after ferrets were infected with influenza B and were given aspirin in combination. Cellular changes were seen, however, after each of these agents was combined with the presentation of the arginine-deficient diet. Intracytoplasmic vacuoles were observed in tissues of the choroid plexus from animals inoculated with influenza B and fed the arginine-deficient diet. Both intercellular vacuolization and intercellular edema were seen in the choroidal epithelia after ferrets were administered aspirin and were fed the synthetic diet. Such cellular changes observed in the choroidal epithelia in response to the paired presentation of these agents were not as severe as those seen in the choroid plexuses of animals in which all three agents were given in combination. These results support the hypothesis that metabolic events that occur after the administration of these agents collectively impact on epithelial cells of the choroid plexus.
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PMID:Response of epithelial cells of the choroid plexus in the ferret model for Reye's syndrome. 382 Oct 66

Viral infections have long been suspected to be causative agents in a number of inner ear dysfunctions. With few exceptions, the virus has not been demonstrated as the direct agent leading to hearing loss and/or vertigo. Selective inner ear changes have been observed recently in sensory and nonsensory epithelial cells in the ferret model for Reye's syndrome after intranasal inoculation with influenza B combined with aspirin administration and the creation of an arginine deficiency. Such findings suggest that these agents act synergistically on the inner ear, particularly on cells that are metabolically active, and that the ferret may now be a useful model to examine the role of certain upper respiratory tract viruses implicated in inner ear disorders, singly and in combination with other agents that may cause metabolic alterations.
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PMID:The ferret as a model for inner ear research. 402 37

A component relatively rich in arginine which was induced by infection with an influenza virus was synthesized in the cytoplasm of the infected cell and migrated to the nucleus. This conclusion was drawn from the grain distribution in autoradiograms and the displacement of (3)H-arginine in isolated cytoplasmic and nuclear fractions after a short pulse and subsequent chase.
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PMID:Cytoplasmic synthesis of an arginine-rich nuclear component during infection with an influenza virus. 516 88

The complete sequence of a hemagglutinin (HA) gene of a recent human influenza A strain, A/Victoria/3/75, is 1768 nucleotides long and contains the information for 567 amino acids. It codes for a signal peptide of 16 amino acids, the HA1 chain of the mature hemagglutinin of 329 amino acids, a connecting region between HA1 and HA2 consisting of a single arginine residue and the HA2 portion of 221 amiino acids. The sequence is compared with the hemagglutinin of two members of other subtypes, the human H2 strain A/Jap/305/57 and the avian Hav1 strain A/FPV/Rostock/34, and with one of the same H3 subtype, A/Memphis/3/72. To align the HA1 chain of different major subtypes several deletions/insertions of single amino acids must be invoked, but two more extensive differences are found at both ends, one leading to an extension of the amino terminal sequence of HA1 and the other (four residues) occurring in the region processed away between HA1 and HA2. Comparison of the HA1 of two H3 strains suggests that drift probably depends on single base mutations, some of which change antigenic determinants. The HA2 region, which apparently is not involved in the immune response, is highly conserved even between different subtypes, and single base substitutions account for all the observed diversity. A hydrophobic segment of 24 residues is present in the same position close to the carboxyl terminus of HA2 in both Victoria and FPV, and presumably functions in implantation into the lipid bilayer. The many conserved features not only in HA2 but also in HA1 suggest a rather rigid architecture for the whole hemagglutinin molecule.
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PMID:Complete structure of the hemagglutinin gene from the human influenza A/Victoria/3/75 (H3N2) strain as determined from cloned DNA. 615 30

A full-length cDNA copy of the neuraminidase (NA) gene of influenza strain A/Tokyo/3/67 was cloned into the plasmid pBR322, and the nucleotide sequence of the gene was determined. In addition, the sequence changes in six variants of A/Tokyo/3/67 selected with various monoclonal antibodies (Ab) to the NA were determined by dideoxy sequencing of the vRNA. In five of the monoclonal variants, a single change occurred, resulting in an amino acid substitution at residue 344. Arginine in the parent virus changed to every amino acid possible with a single nucleotide change. In another variant, arginine at position 253 changed to serine, a change that also occurred in field strains. All variants so far sequenced that were selected by monoclonal Ab to A/Tokyo/3/67 virus changed at position 344, except one which changed at residue 368. Both of these positions are in clusters of residues that vary considerably in field strains, the clusters being 344-347 and 368-370. Analysis of the three-dimensional crystal structure of the NA of A/Tokyo/3/67 shows that these clusters are directly adjacent on the protein, and likely comprise a single antigenic site. A total of three or four antigenic sites have been proposed for the NA protein, based on antigenic mapping with monoclonal Ab [R. G. Webster, V. S. Hinshaw , and W. G. Laver (1982) Virology 117, 93-104]. Variants selected by Ab to Tokyo/67 NA all change in this single antigenic site, whereas variants selected by Ab to other strains change in other regions. It is possible that, although there may be three or four antigenic sites on the NA molecule, there may be a single, dominant antigenic site for each strain.
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PMID:Sequence of the neuraminidase gene of influenza virus A/Tokyo/3/67 and previously uncharacterized monoclonal variants. 620 16

The complete nucleotide sequence has been determined for a cloned double-stranded DNA copy of the haemagglutinin gene from the human influenza strain A/NT/60/68/29C, a laboratory-isolated variant of A/NT/60/68, an early strain of the Hong Kong subtype. The gene is 1765 nucleotides long and contains information sufficient to code for a protein of 566 amino acids, which includes a hydrophobic leader peptide (16 residues), HA1 (328), HA2 (221) and an arginine residue which joins the HA subunits. Comparison of the predicted amino acid sequence for 29C haemagglutinin with protein sequence data available for HA from other influenza strains shows that no potential coding information is lost by processing of the mRNA. A comparison of the amino acid sequences predicted from the gene sequences for 29C and fowl plague virus haemagglutinins, (1) indicates the extent to which changes can occur in the primary sequence of different regions of the protein, while maintaining essential structure and function.
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PMID:Complete nucleotide sequence of the haemagglutinin gene from a human influenza virus of the Hong Kong subtype. 625 83

A synthetic dodecadeoxynucleotide primer has been used to prepare a double-stranded DNA form of the hemagglutinin (HA) gene of a human influenza virus (WSN strain, HON1). This DNA has been inserted in plasmid pBR322 and cloned in bacterial cells. The insert contains nearly the complete hemagglutinin gene. A restriction map of this insert has been determined and structurally important areas of the HA gene have been sequenced. Amino acid sequences of several regions of the HA protein were deduced from the DNA sequences and compared to the known amino acid sequences of other influenza A viruses. WSN HA shows extensive homology to all influenza A viruses in a few regions, namely the first 17 amino acids of the N-terminus of HA1 (N-terminal polypeptide of HA) and the first 24 amino acids of the N-terminus of HA2 (C-terminal polypeptide of HA). The sequence diverges extensively from other influenza A viruses in most other areas. The sequence of WSN virus HA is similar to that of other HON1 viruses with the exception of the C-terminus of the HA1 peptide. The change in this area may contribute to some of the unique properties of WSN virus among the HON1 viruses. In addition, WSN HA contains a 17-amino-acid precursor before the N-terminus of HA1 and a single amino acid, arginine, connecting HA1 and HA2.
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PMID:Construction and characterization of a bacterial clone containing the hemagglutinin gene of the WSN strain (HON1) of influenza virus. 625 39

The individual effects of an influenza B viral infection, aspirin, and an arginine-deficient diet on the inner ear were assessed in the ferret model for Reye's syndrome using both functional and morphological parameters. Auditory brainstem evoked responses recorded from inoculated ferrets revealed threshold elevations and increased latencies during the first 72 hours, but approximated those of control animals by 96 hours. Although there was a mild distention of Reissner's membrane, no pronounced structural alterations in sensory or supporting cells were observed in cochleas from inoculated ferrets. The administration of aspirin appeared to alter neither the functional nor the structural integrity of the cochlea. The presentation of an arginine-deficient diet, creating a hyperammonemic condition, led to both altered auditory evoked responses and vacuolization of cochlear tissues after treated animals had undergone seizures and coma. These data demonstrated that both influenza B and the arginine-deficient diet individually affected the hearing of treated animals. The individual agents did not alter the cochlea as severely as when they were presented in combination. These results suggest that hearing impairment in patients with Reye's syndrome may be a result of potentiation of certain metabolic-altering agents.
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PMID:Effects of influenza infection, aspirin, and an arginine-deficient diet on the inner ear in Reye's syndrome. 650 26

The amino acid sequences and biological properties of the haemagglutinin of three variants of the influenza virus X-31 (H3N2) selected for their capacity to grow in MDCK cells are reported. In two variants, amino acid substitutions at HA1 residues 8 and 144 correlated with the loss of a site for glycosylation and specific changes in antigenicity, respectively. In all three variants substitution of an arginine residue for histidine at HA1 position 17 was correlated with increased pH optima of haemolysis. The importance of this substitution for cleavage of the haemagglutinin precursor required to produce infectious virus is discussed in relation to the three-dimensional structure of X-31 haemagglutinin.
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PMID:Studies on the adaptation of influenza viruses to MDCK cells. 652 17

Recent studies have indicated that viral infections, aspirin treatment and hyperammonemia are associated with Reye's syndrome. It has also been reported that free fatty acids in serum and total lipids in the liver of Reye's syndrome patients are elevated during illness. The role of the lipid changes in the development of the disorder cannot be optimally studied in human patients, because infection and aspirin ingestion occur prior to the earliest symptoms of Reye's syndrome. Effects of influenza B infection, aspirin treatment and hyperammonemia on the level of free fatty acids, total lipids and triacylglycerols in serum and liver of an animal model of Reye's syndrome are reported here. Hyperammonemia was produced in young, male ferrets either by feeding them small amounts of an arginine-deficient diet after overnight fasting or by an intraperitoneal injection of jackbean urease. The ferret model resembled Reye's syndrome in developing increased levels of individual and total serum free fatty acids, liver triacylglycerol and total lipids. The results also indicate that influenza infection or aspirin treatment, or both, while increasing the severity of encephalopathy in the deficient ferrets, did not cause a significant change in the level of serum free fatty acids. Other results suggest that elevation of serum ammonia, serum free fatty acid or liver lipids, either singly or in various combinations, does not provide conditions that can explain the rapidly developing encephalopathy in the arginine-deficient ferrets.
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PMID:Free fatty acids in an animal model of Reye's syndrome. 661 53


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