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Results for “NEURAMINIDASE”

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PubMed1979

Autoimmune reactions against liver cells by syngeneic neuraminidase-treated lymphocytes.

We have found that the entrapment of neuraminidase-treated lymphocytes in the liver leads to the induction of autoimmune cellular cytotoxic reactions. Lymphocytes from mouse spleen and thymus were incubated with neuraminidase in vitro and injected i.v. into syngeneic recipients. Lymphocytic infiltrations into the liver were seen 7 days later with both types of cells. After repeated weekly injections of asialo-lymphocytes, destruction of liver tissue became apparent. Electron-microscopic studies showed that hepatocytes, fat storage cells, and endothelial cells were affected, mainly at the hepatic periphery. It is concluded that the adhesion of asialo-lymphocytes to liver cells induces their cytotoxic activity. Similar reactions may occur after paramyxovirus infection due to the action of viral neuraminidase.

Animals↗

PubMedDate not supplied

[Influenza virus neuraminidase and its role in anti-influenzal immunity].

The direct relationship between immunogenicity of H3N2 formolvaccine and neuraminidase activity was established. A single intranasal immunization of mice with the vaccine having a titer of hemagglutinin 1:20,000-1:40,000 in 0.5 ml with active neuraminidase increased the resistance of the animals to the challenge with mouse-adapted influenza A/USSR/053/74 (H3N2) virus almost 5-fold. A vaccine with the same hemagglutinin titer but with neuraminidase inactivated by physico-chemical factors or blocked by specific antibody exerted a protective effect 2.5-3 fold weaker than the vaccine with the active enzyme.

Animals↗

PubMed1981

Colony formation by bone marrow cells after incubation with neuraminidase. II. Sensitivity of erythroid progenitor cells for burst promoting activity and erythropoietin and restoration of reduced spleen colony formation in mice pretreated with desialated erythrocyte membrane fragments.

Incubation of bone marrow cells (BMC) with neuraminidase (NA) reduces their ability to form colonies in the spleen of lethally irradiated mice. In vivo the largest reduction was observed in the erythrocytic colonies, whereas in vitro an inhibiting effect of NA incubation was observed on the plating efficiency of erythrocyte precursors (CFUE and day 7 BFUE). Masking of the receptors for neuraminidase-treated cell surface determinants in the recipient's body by infection of desialated erythrocytes (NA-Ery) or erythrocyte membrane fragments (NA-Efr) did largely restore the reduced colony formation of NA-BMC with respect to both the total number of spleen colonies and their type. Pretreatment of irradiated host with NA-Ery, but with NA-Efr, led to a slight polycythemia as judged by the number of erythrocytic and undifferentiated colonies as well as by the surface colony diameter. The reduced erythrocytic colony formation of NA-BMC was considerably enhanced in anemic irradiated recipients (from 25-70% of respective controls). Under all experimental circumstances the erythrocytic colony formation of NA-BMC never exceeded that of normal BMC (N-BMC). Further, in normal or anemic recipients whether or not treated with NA-Efr, the diameters of the spleen surface colonies in NA-BMC injected animals were smaller than in recipients of control-incubated BMC. In vitro experimentation indicated that the reduced plating efficiency of CFUE and BFUE following incubation could not be attributed to a decreased sensitivity to erythropoietin. However, day 7 BFUE with deficient cell surface sialic acid residues had a decreased sensitivity to burst promoting activity. Among several other explanations, our data support the possibility that the desialated colony forming cells that give rise to erythrocytic colonies in vivo have higher requirements for early regulatory factors than granulocytic precursor cells. In contrast to the normal postirradiation situation the level of these factors could be increased in recipients, which are bled subsequently to irradiation. Evidence is presented in support of our concept that neuraminidase-treated CFU are fully capable to exhibit normal, although delayed, colony formation in vivo in animals with covered receptors for galactosyl residues.

Animals↗

PubMed1980

Some properties of mumps virus neuraminidase.

Mumps virus strains were characterized by the neuraminidase activity of infected allantoic and amniotic fluids of chick embryos. Ovomucoid was used as substrate for determination of neuraminidase activity. Storage of virus samples at 4 degrees C led to great losses of enzyme activity. Alkali chlorides, divalent cations, EDTA and N-ethylmaleimide exerted a low to medium inhibitory activity. Surfactants, depending on their type, caused inhibition, activation or no effect on the enzyme--substrate reactions. The pH optimum was 5.6 and 5.3 with mumps virus strains Enders and Jeryl Lynn, respectively. The Michaelis constants of 9.43 X 10(-3) and 7.57 X 10(-3) mol/1 allowed a differentiation of the two mumps virus strains based on their neuraminidase.

Animals↗

PubMed1981

Interferon induction by influenza virus: significance of neuraminidase.

During interferon induction in mice in vivo with various strains of influenza A virus differences in titer of produced interferon were observed. Correlation between interferon titer and neuraminidase activity of a given influenza virus strain was noted. Similar correlation was demonstrated with virus fraction purified chromatographically and used for interferon induction. The fractions with high neuraminidase activity were good interferon inducers, whereas the fractions with undeterminable neuraminidase activity did not induce interferon in vivo.

Animals↗

PubMed1982

[Inhibitory effect of combined administration of neuraminidase and interferon in mice with Rauscher leukemia].

A study was made of the effect of cholera vibrio neuraminidase and mouse interferon on the development of Rauscher's leukemia in BALB/c mice. It was shown that administration of 1500 units interferon to mice 4 hours before and 5 days after inoculation of Rauscher's leukemia virus prolonged the animals' lifespan. Preliminary treatment of the virus-containing material with neuraminidase prevented the death of one third of the experimental animals. Meanwhile the remainder of the animals inoculated with the same virus showed a longer lifespan. Combined use of both the preparations proved the most effective, enabling the prevention from death of 90% of the experimental animals. The mechanism of antiviral action of neuraminidase and interferon is discussed.

Animals↗

PubMedDate not supplied

[Antigenic heterogeneity of influenza virus B neuraminidases].

Antigenic relationships among neuraminidases of influenza B viruses isolated in 1940-1980 were studied by means of the neuraminidase activity inhibition test using hypoimmune sera from rats and roosters. Cross-reactions between influenza B virus enzymes showed their antigenic heterogeneity. The results permit conclusion that among influenza B virus strains both the drift and shift variants may be distinguished by the antigenic composition of the neuraminidase component.

Animals↗

PubMedDate not supplied

[Determination of the antigenic specificity of the neuraminidase of influenza viruses].

The principal possibility of using beta-propiolactone-inactivated and lyophilized antigens of influenza A and B viruses and of mouse immune ascitic fluids to them for the determination of the antigenic specificity of neuraminidase has first been established. A simpler and easier method requiring no expensive reagents: inhibition of influenza virus release from erythrocytes was tested. This method is as specific as the labour-consuming and difficult test of neuraminidase activity inhibition, and allows a rapid and accurate identification of the type of neuraminidase of influenza viruses of various origins to be made.

Animals↗

PubMed1981

Neuraminidase activity and cell surface sialic acid turnover in Rous sarcoma virus transformed chick embryo fibroblasts.

Neuraminidase activity of Rous sarcoma virus transformed chick embryo fibroblasts (RSV-CEF) was assayed using an exogenous substrate, neuraminlactitol-[3H], and endogenous, cell surface [14C]-N]-acetyl-neuraminic acid. RSV-CEF had higher neuraminidase activity toward both substrates than did chick embryo fibroblasts (CEF) or nontransformed, Rous associated virus infected CEF (RAV-CEF). The total sialic acid content of RSV-CEF was lower than CEF or RAV-CEF, and more of the total sialic acid was accessible to extracellular Clostridium perfringens neuraminidase. Activity of the enzymes synthesizing and degrading the substrate for sialyltransferase, cytidine-5'-monophosphate-N-acetyl-neuraminic acid (CMP-AcNeu) was measured in order to determine whether control of substrate levels for sialyltransferase might contribute to the decreased levels of glycoprotein bound sialic acid. No change in activity of these enzymes was found in RSV-CEF as compared to CEF or RAV-CEF.

Animals↗

PubMed1978

[Changes in the antigenicity of influenza virus neuraminidases due to various methods of preparation].

The influenza virus strains A/Sing/1/57 (H2N2), A/Bel/42 (HoN1) and A/Bel/42 (Ho)-A/Sing/1/57 (N2) were treated with bromelain under reducing conditions and with reducing agent alone, and the antigenicity of the neuraminidase (NA) of intact virus and of the split products was tested comparatively. It was found that the antigenicity of NA was influenced quantitatively and qualitatively by the preparation procedure. Antineuraminidase (AN) antibodies obtained after vaccination of guinea pigs with intact virus and with split products differed in their cross-reactivity with heterologous neuraminidases. AN antibodies directed against N2 NA on the recombinant differed qualitatively from those directed against N2 NA of parent virus. The results warrant the conclusion that the antigenicity of isolated NA or of NA on recombinant virus can differ from that of the NA on intact homologous virus and that such alterations could influence the determination of antigenic relationship between neuraminidases.

Antibodies, Viral↗

PubMed1981

Augmentation of the antibody forming cell response to neuraminidase-treated cells by myxoviruses.

Following the inoculation of Newcastle Disease virus, Sendai virus and influenza virus CBA mice made a specific plaque-forming cell response to virus-treated sheep red blood cells but not to virus-treated L1210 cells. This non-specific response to virus-treated L1210 could be exactly reproduced by treatment of L1210 with bacterial neuraminidase. Neuraminidase-treated cells from eight of nine vertebrates including chickens and syngeneic mice also registered plaques. Inoculations of the above viruses were considered to have evoked separate antibody forming cell responses to viral antigens, foreign cell components in the virus inoculum and to neuraminidase revealed cell membrance antigens.

Animals↗

PubMed1984

Neuraminidase production by Candida albicans.

A Candida albicans strain G42, isolated from a vaginal infection, was demonstrated to produce neuraminidase in culture filtrates with activity for N-acyl-neuraminic acid glycoprotein from bovine submaxillary gland, and human erythrocytes as substrates. Incubation of viable cells from G42 with human group O Rh(+) erythrocytes released N-acetyl-neuraminic acid in a time-dependent manner. Thirty-two clinical isolates of C albicans were studied for neuraminidase production. Enzyme activity was found in culture filtrates from five strains.It would appear important from these data to determine whether the production of neuraminidase by C albicans can be correlated with pathogenicity.

Animals↗

PubMed1982

[Role of enterotoxin and neuraminidase in the biological activity of E1 Tor vibrios].

The biological activity of the toxigenic strains of cholera vibrios in suckling rabbits used as a model is manifested irrespective of the amount of neuraminidase produced by these strains. Neuraminidase is important only in low-cholerogenic strains, which is confirmed by a significantly greater death rate among suckling rabbits infected with cultures producing 40-2560 ng/ml of the exoenzyme in comparison with that among suckling rabbits infected with strains producing less than 10 ng/ml of the exoenzyme, or not producing it at all. The relation between the amounts of enterotoxin and neuraminidase, produced in vitro, and the biological activity of strains in suckling rabbits has been established, which allows one to study the virulence of strains in the passive immune hemolysis and aggregate hemagglutination tests.

Animals↗

PubMed1982

Galatosialidosis (beta-galactosidase-neuraminidase deficiency): clinical and biochemical studies on 13 patients.

Thirteen patients with galactosialidosis (beta-galactosidase-neuraminidase deficiency) from 9 families including two autopsy cases were studied from clinical, genetic, cytological and biochemical standpoints. Coarse facies, myoclonus, cerebellar ataxia, angiokeratoma, loss of vision, corneal opacity and cherry-red spots were the main signs and symptoms although these clinical manifestations were widely variable in individual cases. It is not yet known whether these clinical variations represent genetic heterogeneity or not. Deficiency of beta-galactosidase and neuraminidase was the most prominent biochemical abnormality in this disease. Beta-Galactosidase activity was restored in fibroblasts when serine-thiol protease inhibitors were added to the culture medium. Cathepsin B activity was significantly high in fibroblasts, liver and brain from the patients. It was demonstrated that neuraminidase was susceptible to the procedures for disrupting cells and tissues, such as sonication and freezing. The stability of this enzyme may be dependent on the molecular state in relation to cell membranes.

Adult↗

PubMed1983

Histochemical demonstration of neuraminidase effects in pneumococcal meningitis.

In three cases of pneumococcal meningitis the in vivo action of pneumococcal neuraminidase could be demonstrated. The removal of sialic acid was demonstrated in necrospy material by the use of labeled peanut agglutinin, which has a high specific affinity for the subterminal disaccharide beta-D-galactopyranosyl-(1-3)N-acetyl-D-galactosamine, thereby exposed. Furthermore, this lectin was used for a rapid in vitro histochemical assay of neuraminidase activity in cerebrospinal fluid and culture medium taken from these cases. From the clinical point of view the exposure of the disaccharide which represents the immunodominant group of the Thomsen-Friedenreich antigen may induce immunologic reactions, because all human sera contain antibodies to this cryptic antigen. Thereby, neuraminidase can contribute to the poor prognosis of pneumococcal meningitis.

Choroid Plexus↗

PubMedDate not supplied

[pH-dependent hemolytic and neuraminidase activity of remantadine-sensitive and -resistant variants of influenza virus].

A comparative study of pH-dependence of hemolytic and neuraminidase activities of four remantadin-sensitive influenza A virus strains CAPV (classical avian plague virus) (H7N7), USSR/090/77 (H1N1), Ann Arbor (H2N2), and Texas (H3N2) and their remantadin-resistant variants was carried out. The original strains were shown to produce hemolysis in a narrow pH range (5.0 and 5.5) and to have maximal neuraminidase activity at the same pH values. In remantadin-resistant variants the optimal pH values for hemolytic and neuraminidase activities were higher by 0.5-1.0 than for the sensitive variants.

Adamantane↗

PubMedDate not supplied

[Enzyme activity of the neuraminidase from various strains of the influenza A virus].

Some chemical properties of neuraminidase of the mouse-pathogenic strain A/PR/8/34 (H0N1) and the mouse-apathogenic strain A/Krasnodar/101/59 (H2N2) were studied. Neuraminidase of the pathogenic strain was shown to have a lower specific activity, lower resistance and lower sensitivity to the inhibiting effect of CI ions than neuraminidase of the nonpathogenic strain.

Animals↗

PubMed1980

Increased proportion of Fc gamma and Fc mu positive T-lymphocytes following treatment with neuraminidase.

Membrane receptors for IgG (Fc gamma) and IgM (Fc mu) were assessed on isolated peripheral blood T-lymphocytes by rosette formation with ox-RBC coated with rabbit IgG or IgM antibodies. The mean percentage of Fc gamma and Fc mu rosettes on freshly separated T-cells was 19% (+/- 6% SD) and 4% (+/- 1% SD), respectively. These values increased significantly to 40% (+/- 9%) for Fc gamma and 34% (+/- 8%) for Fc mu after preincubation of the lymphocytes with Neuraminidase. The proportion of Fc mu, but not of Fc gamma, rosettes increased to 44% (+/- 8 SD) after overnight incubation at 37 degrees C, and less markedly after incubation for 45m at 37 degrees C (29% +/- 7). Fc gamma and Fc mu rosette formation, with or without neuraminidase, was specifically inhibited by human IgG or IgM. These findings suggest (1) that hidden receptors can be demonstrated on T-lymphocytes after Neuraminidase treatment which, in the case of Fc gamma, cannot be revealed by other means, and (2) that the proportion of T gamma lymphocytes in the peripheral blood is higher than generally believed.

Animals↗