Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In native, heated or otherwise treated egg white and in sera of men and guinea pigs, haemagglutination inhibition titres were determined against three inhibitor-sensitive (IS) strains and one inhibitor-resistant (IR) variant on influenza A virus. A few human sera with no detectable antibody revealed high inhibition titres even against the IR variant. Human sera after treatment with trypsin and periodate revealed mostly a reduction or no change, and exceptionally an increase of their inhibition titre. The extent of these changes varied with different influenza virus strains and showed a positive correlation with the inhibitor content and no correlation with the antibody levels of the sera. The so-called "nonspecific" thermostable inhibitors possess a certain degree of specificity for different influenza virus strains.
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PMID:Detection of "alpha-type" inhibitors in the presence of low levels of specific influenza antibodies. 3 34

Using M-TUR, a macrophage-adapted avian influenza A virus (Hav1, Nav3), antiviral resistance of peritoneal macrophages obtained from specifically or nonspecifically immunized mice towards in vitro infection was assessed. M-TUR grew to high titers in macrophages from nonimmune mice thereby causing a marked cytopathic effect. In contrast, peritoneal macrophages from mice specifically immunized with TUR virus were not affected by infection with M-TUR in vitro. This antiviral immunity was specific: mice immunized with antigenetically unrelated influenza strains such as influenza A/Hong Kong/1/68 (H3, N2) or influenza B/Lee yielded susceptible macrophages. Specific macrophage immunity could be abrogated by trypsin treatment in vitro. Susceptible macrophages from nonimmune hosts became resistant following in vitro exposure to homologous anti-TUR sera. Peritoneal exudate cells from BCG-infected animals were less susceptible to in vitro challenge with M-TUR than control macrophages. In vivo treatment of mice with the unspecific immunostimulants BCG or Corynebacterium parvum did not protect the animals against lethal infection with a hepatotropic variant of TUR.
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PMID:Macrophage immunity to influenza virus: in vitro and in vivo studies. 8 51

Various strains of influenza C virus grew productively in an established line of monkey kidney cells (LLCMK2) without prior adaptation. When trypsin was added to the medium, higher virus yields were obtained than in other cell cultures. All influenza C virus strains tested formed well defined plaques under the agar overlay medium containing trypsin. Infectivity determined by plaque assay in LLCMK2 cells was higher than that determined by amniotic inoculation of fertile hens' eggs.
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PMID:Established cell line sensitive to influenza C virus. 11 96

The usefulness of some cells cultures (BSC-I, VERO, MDSK) for isolation and study of reproduction of influenza A viruses was explored. Out of 50 clinical specimens examined, in 16 cases the virus was isolated both in chick embryos and in MDSK cell cultures. MDSK cultures were found to be highly sensitive to influenza A viruses, which produced cytopathic effect and hemagglutinin accumulation. The plaques formed by freshly isolated strains under an agar overlay containing trypsin were markedly polymorphous. MDSK cells may be recommended for use in virus isolation studies. Examinations of virion morphology revealed their diversity both in size and shape.
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PMID:[Isolation and study of influenza A viruses in different cell cultures]. 11 39

A survey of over 600 'normal' sera from 14 animal species by immunoprecipitin tests in cellulose acetate using viron antigens revealed a high incidence of precipitating activity against a broad range of influenza A virus strains, particularly A2hHong Kong/1/68 and /PR8. However, serum treatments trypsin-heat-periodate, NaIO4, V. cholerae receptor-destroying enzyme (RDE), or kaolin eliminated most precipitating activity, which suggests that it was due to "non-specific" inhibitors of influenze viruses. A resistant minority could not be identified as inhibitor or antibody on this basis. Precipitation of the influenza A major type-specific antigen in virus-soluble antigens by human 7S gamma globulin antibody (IgG), demonstrated to be specific for influenza virus, was established as a reference reaction to identify similar immunoprecipitin reactions occurring between virus-soluble antigens and normal or immune sera. Complement fixation tests provided supplementary evidence for the presence of influenza A antibodies in these sera. Influenza A antibodies were found in only a few sera of six animal species: cat, dog, rabbit, goat, chipmunk, and sheep. Thus the animal species examined in the Ottawa area have not revealed an unequivocal reservoir for human influenza A viruses.
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PMID:An immunoprecipitin study of the incidence of influenza A antibodies in animal sera in the Ottawa area. 16 31

Fusion of red blood cells (RBC) induced by hemagglutinating virus of Japan (HVJ) has been studied using a phosphatidylcholine spin label. The spin label was readily incorporated and diffused into the lipid bilayer portion of the viral envelope. The exchange broadening in the electron spin resonance (ESR) spectrum of densely labeled virus disappeared rapidly when the virus was mixed with RBC at 37 degrees. The spectrum gradually approached that of the host cell spin labeled with the phosphatidylcholine label. The results directly indicate transfer and intermixing of phospholipid molecules between the viral envelope and RBC membrane. The transfer reaction was strongly dependent on temperature. No transfer was observed at lower temperatures where the virus adsorbed to the cell and caused aggregation but no hemolysis and fusion. The transfer rate remained negligibly small until 19 degrees and increased rapidly between 25 and 30 degrees. The virus-induced hemolysis showed similar temperature dependence. The transfer rate was greatly reduced under inhibitory conditions of fusion: glutaraldehyde treatment of RBC, trypsin treatment of HVJ, or the presence of concanavalin A. Only slight transfer was observed from fusion-inactive influenza virus to RBC. The transfer was greatly enhanced by the help of HVJ. The close parallelism suggests that the transfer and intermixing are necessary steps to the cell fusion. The transfer rate was dependent on fluidity of the host cell membrane and independent of the viral dose. The virus-induced transfer of phospholipid molecules between RBC's was also detected by the spin label. Its temperature dependence was quite similar to that for the virus-to-cell transfer. The intercellular transfer was nearly proportional to the viral dose.
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PMID:A spin-label study on fusion of red blood cells induced by hemagglutinating virus of Japan. 16 84

Transfer of phospholipid from the envelope of hemagglutinating virus of Japan (HVJ) to erythrocyte (RBC) membrane and the virus-induced transfer of phospholipid between RBC membranes were studied using spin-labeled phosphatidylcholine (PC). The transfer of PC from membranes labeled densely with PC to unlabeled membranes was followed by the peak height increase in the electron spin resonance spectrum. The two kinds of transfer reactions took place very rapidly as reported previously. To obtain further details, the transfer reactions were studied with HVJ, HVJ inactivated by trypsin, HVJ harvested early, HVJ grown in fibroblast cells, the fibroblast HVJ activated by trypsin, influenza virus, and glutaraldehyde-treated RBCs. The results demonstrated that the viral F glycoprotein played a crucial role in the transmembrane phospholipid movements as well as in the fusion and hemolysis of RBCs. The transfer from HVJ to RBC's occurred partially through an exchange mechanism not accompanying the envelope fusion. This was shown by a decrease in the exchange broadening of the electron spin resonance spectrum of released spin-labeled HVJ (HVJ) and also by an increase in the ratio of PC to viral proteins incorporated into RBC membranes. HVJ modified RBC membrane so as to be able to exchange its phospholipids with those of inactive membranes such as fibroblast HVJ, influenza virus, glutaraldehyde-treated RBC'S, and phosphatidylcholine vesicles. HVJ affected the fluidity of RBC membranes markedly, the environments around PC being much fluidized. The virus-induced fusion was discussed based on close apposition of the membranes by HANA proteins and on the destabilization and fluidization of RBC membranes by F glycoproteins.
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PMID:Transmembrane phospholipid motions induced by F glycoprotein in hemagglutinating virus of Japan. 18 66

The results of studies of the quantitative values of nonspecific antihemagglutinins of influenza viruses in the sera of birds, laboratory, wild and domestic animals (altogether 27 species) are presented. The antiviral inhibitors characterized by a number of physicochemical properties (sensitivity to heating, KIO4, trypsin, rivanol, 2-mercaptoethanol) were divided into 3 groups, sera of sheep, goats and cattle making up a separate group with regard to their sensitivity to heating and treatment with KIO4. Studies using molecular screen chromatography demonstrated the nonspecific inhibitors present in bovine sera to be heterogenous both in type (thermolabile and thermostable) and in the molecular composition. Alongside with thermolabile inhibitors of macroglobulin nature, thermostabe 19S and 4S inhibitors were identified.
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PMID:[Quantitative indices and physico-chemical properties of non-specific inhibitors of influenza A virus hemagglutination in the sera of different species of animals and birds]. 19 65

By means of a continuous canine kidney cell line (MDCK), influenza viruses were rapidly isolated from specimens collected from patients with respiratory disease. The cell line proved more sensitive than either eggs or rhesus monkey cells for currently circulating influenza A and B strains. Influenza viruses caused a distinct cytopathology within 5 days of inoculation if trypsin-ethylenediamine-tetraacetic acid was incorporated into the medium. Sufficient hemagglutinin was produced on the initial tissue culture passage to allow direct identification of isolates by hemagglutinin inhibition tests. A variety of other respiratory viruses replicated in MDCK, and over a 10-month period 211 of 600 specimens (35%) yielded viruses.
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PMID:Canine kidney cell line for isolation of respiratory viruses. 21 21

Peripheral blood leukocytes, obtained from volunteers after vaccination or natural illness with influenza, were assayed for cytotoxicity against influenza virus-infected cells. Approximately 7 days after vaccination or the onset of respiratory illness, peak cytotoxicity was demonstrated in a chromium-release assay. Secretion of specific antibody against hemagglutinin from the leukocytes during in vitro incubation was demonstrated in quantities that would mediate the cell cytotoxicity observed. Antibody secretion was inhibited by exposure to cycloheximide but not by exposure to trypsin. The secretion of antibody against hemagglutinin from peripheral blood leukocytes occurred only at the time of maximal cytotoxicity. We thus demonstrate secretion of specific antibody in vitro after recent viral antigen stimulation. Moreover, this antibody is capable of conveying cytotoxic capacity to peripheral blood leukocytes that may be important in the recovery process from acute viral infection.
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PMID:Cell cytotoxicity due to specific influenza antibody production in vitro after recent influenza antigen stimulation. 29 90


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