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

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

Exposure of vesicular stomatitis (VS) virions to neuraminidase resulted in loss of their ability to agglutinate goose erythrocytes and to attach to L cells concomitant with hydrolysis of sialic acid. These viral adsorptive functions were also destroyed by tryspsinization. Sialyl transferase resialylation in vitro of neuraminidase-treated VS virions restored their hamagglutinating and adsorptive functions almost to original levels. Erythrocyte and L cell receptors for attachment of VS virions were blocked by fully sialylated fetuin and by VS viral sialoglycopeptides. Smaller VS viral glycopeptides generated by extensive trypsinization were less effective inhibitors of hemagglutination than were larger glycopeptides; neuraminic acid and neuraminosyl lactose had no capacity to inhibit hamagglutination or adsorption of virus to L cells. These data suggest that cellular receptors for viral adsorption recognize sialoglycopeptides of a certain size. Neuraminidase desialylation did not significantly alter the isoelectric point of VS virions. Cells exposed to DEAE-dextran, trypsin, or neuraminidase showed significantly increased capacity to attach fully sialylated but not desialylated VS virions. Neuraminidase desialylation of L cells, Chinese hamster ovary cells, and Madin-Darby bovine kidney cells resulted in enhanced susceptibility to plaque formation by VS virus.
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PMID:Cellular adsorption function of the sialoglycoprotein of vesicular stomatitis virus and its neuraminic acid. 16 24

By treatment of chorioallantoic membranes from embryonated eggs with collagenase and hyaluronidase before the conventional application of trypsin cells could be grown in culture which supported growth of a large variety of myxoviruses, herpesviruses, avian reoviruses and the infectious bronchitis virus of chickens. The cultures could be used for sensitive plaque assays and neutralization tests.
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PMID:In vitro cultivation of cells from the chorioallantoic membrane of chick embryos. 16 93

When a 24-h tube culture of rabbit alveolar macrophages was infected with Sendai virus, the rate of infected cells was found to be limited. Even at a multiplicity of infection (MOI) of 500 plaque-forming units per cell, an average of 63% cells was found to synthesize viral antigens stainable by direct immunofluorescence. When the macrophages obtained from rabbits hyperimmunized by an intravenous injection of Sendai virus were infected under the same in vitro conditions, the rate of antigen synthesis averaged a low as 23%. At the time of infection of alveolar macrophages from immunized rabbits (immune macrophages), cell aggregation at an MOI 50 and cell fusion at an MOI 500 were found 24 h after infection, and these reactions were never encountered after the infection of nonimmune macrophages. When the immune macrophages were either pretreated by trypsin or incubated in medium at pH 4.0, the infection no longer caused the aggregation. The supernatant fluid obtained after incubation at pH 4.0 contained neutralizing antibody to Sendai virus. Conversely, when nonimmune macrophages were incubated in the presence of rabbit anti-Sendai virus serum or purified immunoglobulin G, the same aggregation reaction occurred after virus infection. Ultraviolet light-killed Sendai virus could be used as the counterpart of alive virus in the same aggregation reaction. These results suggest that the aggregation reaction of the immune macrophages could be attributed to the presence of specific cytophilic antibodies on their surface.
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PMID:Specific macrophage immunity to Sendai virus: macrophage aggregation in vitro with Sendai virus by cytophilic antibodies. 16 54

Systematic studies on the replication of varicella-zoster virus in infected human fetal diploid lung cells have defined more optimal conditions for infection and harvesting of cultures and have led to the production of cell-free virus preparations with infectivity titers of greater than or equal to 10(6) plaque-forming units per ml. The highest yields of cell-free virus were obtained by (i) sonic treatment of the cellular phase of cultures inoculated with trypsin-dispersed infected cells at ratios of 1 infected cell to 6 to 10 uninfected cells in the monolayer and (ii) harvesting cells after 24 to 36 h of incubation at 36 degrees C. At this time the cultures showed minimal viral cytopathic effect. Spread of infectivity occurred much more rapidly in cultures inoculated with whole infected cells than in those infected with cell-free virus. Complement-fixing antigens with improved titers of greater than or equal to 1:128 were prepared from varicella-zoster virus-infected cell cultures in the same manner as cell-free virus, but harvested after 3 to 4 days of incubation when the cultures showed an advanced cytopathic effect.
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PMID:Improved yields of cell-free varicella-zoster virus. 18 51

Neonatal calf diarrhea virus (a bovine rotavirus) formed distinct plaques in monolayers of MA-104 cells, an established macacus rhesus monkey kidney cell line, when diethylaminoethyl dextran and trypsin were included in the overlay medium. By using this plaque assay method, titration of neutralizing antibody to neonatal calf diarrhea virus was made feasible. It was demonstrated that some human sera contained neutralizing antibody to this agent.
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PMID:Plaque assay of neonatal calf diarrhea virus and the neutralizing antibody in human sera. 18 63

Cell lines derived from human malignant melanoma tumors are susceptible to infection with varicella-zoster virus (VZV). Within 5 days after inoculation of vesicular fluid, cytopathic changes appeared in melanoma cell monolayer cultures that were incubated at either 36 or 32 degrees C. The VZV isolates at the two temperatures were serially propagated by passage of trypsin-dispersed infected cells. A plaque assay was developed utilizing melanoma cell monolayers overlaid with nutrient medium containing carboxymethylcellulose. By this assay method, the growth cycle of a VZV isolate propagated at 36 degrees C was studied and compared with that of another VZV isolate grown at 32 degrees C. With equivalent infected-cell inocula at a ratio on one inoculum cell to eight uninfected cells, the yield of cell-free virus at an incubation temperature of 32 degrees C was slightly higher than at 36 degrees C, although the peak occurred 60 h, rather than 36 h, postinfection. It was also found that the titer of low-passage VZV propagated at 36 degrees C was 0.5 to 1 log higher when assayed at 32 degrees C rather than at 36 degrees C.
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PMID:Varicella-zoster virus: isolation and propagation in human melanoma cells at 36 and 32 degrees C. 20 32

Primary and secondary cultures of rhesus monkey kidney cells supported multiple-cycle replication of Sendai virus, but later passages lost this ability, and this was reflected in decreased plaque formation. Multiple-cycle replication also did not occur in LLC-MK2 cells, a continuous line of RMK cells. Failure of replication in serially passed cells was correlated with a decrease in proteolytic cleavage of a viral surface glycoprotein (Fo), and the ability of cells to support multiple-cycle replication and plaque formation could be restored by the addition of trypsin (0.3 microgram/ml) to the overlay medium. The use of wild-type virus, which requires trypsin, and protease activation mutants that require chymotrypsin or elastase for activation has provided evidence that the activating protease supplied by primary or secondary cells has trypsin-like activity. Inactive virus, with uncleaved Fo glycoprotein, absorbed to primary or secondary cells but did not infect them, even though such cells possess the enzyme that is capable of cleaving the Fo glycoprotein of virus synthesized in these cells. The inability of these cells to activate adsorbed virus indicates that the activating protease that they possess is inacessible to adsorbed virus, although it can act on the Fo glycoprotein during virus maturation in these cells. These data provide a biochemical explanation for the failure of later passages of a cell strain or a continuous cell line to support the replication of a paramyxovirus.
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PMID:Loss on serial passage of rhesus monkey kidney cells of proteolytic activity required for Sendai virus activation. 20 71

A sensitive, quantitative and reproducible plaque assay for the measurement of the simian rotavirus SAII is described. Plaque formation required the presence of the facilitators pancreatin or trypsin and diethylaminoethyl-dextran in the agar overlay. SAII produced plaques in three continuous primate cell lines: MA-104, CV-1 and LLC-MK2. MA-104 cells were the most sensitive.
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PMID:A plaque assay for the simian rotavirus SAII. 22 32

The lymph node viable cells suspension of immunized mice was centrifugated. The supernatant was chromatographed in Sephadex G-200, and fractions were deproteinized. The deproteinized third fraction (Mol wt 30000) stimulated specifically the plaque-forming cells of intact mice immunized by SRBC. It restored the capacity to antibody production in the lethally irradiated intact mice protected by the syngeneic bone marrow. The activity of this fraction disappeared following treatment with RNA-ase, but not with DNA-ase or trypsin. The first and the second deproteinized fractions of the supernatant inhibited non-specifically the viable lymph node cells of the immunized animals in the intact mice immunized with SRBC.
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PMID:[Replacement of the helper function of T cells by an RNA-containing antigen-specific lysis factor]. 31 Dec 27


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