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Biomedical subjects

G Rutter

Publications and source records attributed to G Rutter.

At least 55 records · Page 3Linked to original sources
PubMed1978

Derivatized silica spheres as immunospecific markers for high resolution labeling in electron microscopy.

For high resolution labeling of influenza virus cell surface antigens on HeLa cells, an immunospecific marker is used with silica sphere cores of 13--14 nm average diameter. These markers are formed using commercially available silica sphere sols. Two other size ranges are available, 7--8 nm and 22--25 nm. The steps for chemical derivatization are described in detail. Amino and aldehyde functions are covalently introduced onto the sphere surface. Sols of these derivatized silica spheres (DSS) are physicochemically stable and therefore usable for years. Coupling of IgG to DSS followed by permeation chromatography on controlled pore glass results in size-defined immunospecific silica sphere markers (DSS-markers). Saturation labeling of cell surface antigens on HeLa cells on cover slips is obtained with the final sphere concentration of 10(14) DSS-marker/cm3 within 20 min. With usual protective conditions, the marker stability and labeling ability are preserved for months. The visibility and the fine structure of the DSS-marker on cell surfaces are shown by using transmission electron microscopy (TEM) with stereo replicas and ultrathin sections.

Antigens, Surface↗
PubMed1977

Alterations of actin-containing structures in BHK21 cells infected with Newcastle disease virus and vesicular stomatitis virus.

The distribution pattern of actin-containing structures in BHK21 cells and the changes which they undergo upon infection with Newcastle disease virus (NDV) and vesicular stomatitis virus (VSV) were studied by means of immunofluorescence. Double labelling with antibodies conjugated with fluorescein (for actin) and rhodamine (for virus antigens) has shown that the progressive cytopathic effects after virus infection are accompanied by extensive alterations of the structures demonstrable by antiactin antibodies. In NDV-infected BHK21 cells the number of actin filaments increases, some zones which contain virus antigens apparently being in close association with the actin structures. By contrast, infection with VSV results in a strong reduction of actin-containing fibres. The results indicate that in the genesis of morphologically detectable alterations of a cell after virus infection--the 'cytopathic changes'--alterations of those structural elements are involved which are also probably responsible for maintenance of cell shape and motility.

Actins↗
PubMed1976

Lymphocytic choriomeningitis virus. II. Characterization of extractable complement-fixing activity.

Lymphocytic choriomeningitis (LCM) virus-specific complement-fixing (CF) antigen (ECFA) has been solubilized, concentrated, and partially purified. When inoculated together with Freund's adjuvant, ECFA induced CF antibody but not neutralizing antibody or protective immunity. By itself it boosted pre-existing CF antibody but no neutralizing antibody. In double diffusion tests one line developed between ECFA and its antiserum, and a corresponding line became visible when ECFA interacted with an antiserum directed against all LCM virus-specific antigens. Absorption of either serum with ECFA abolished all ECFA-precipitating qualities. Ouchterlony tests also revealed that ECFA prepared from cells and tissues of various species is immunologically identical. By a variety of procedures ECFA was not found to be represented on the surface of either the virion or the infected cell. When purified infectious LCM virus was disrupted, a CF antigen corresponding immunologically to ECFA was set free. In double diffusion tests this antigen gave a line of identity with ECFA. Thus, ECFA appears to be an internal component of the infectious LCM virus.

Animals↗
PubMed1976

Antibody-induced redistribution of virus antigens on the surface of influenza virus-infected cells.

The behaviour of virus-specific antigen-antibody complexes at the plasma membrane of HeLa cells infected with influenza virus (A0PR8) was studied by immunofluorescence- and immunoelectron-microscopy. As early as 7 h after infection the virus-induced plasma membrane antigens are evenly distributed over the surface of the infected cells. The addition of antiviral antibodies interferes with this distribution. The appearance of a subsequent patchlike and 'capping' distribution, followed by the disappearance of virus antigen-antibody complexes from the cell surface, is described. These findings demonstrate the potential mobility of virus-induced antigens in the plane of the cell surface.

Antibodies, Viral↗
PubMed1975

Use of iodinated organic compounds for the density gradient centrifugation of viruses.

Use of Urografin and Conray for the equilibrium centrifugation of viruses is described. These pharmaceuticals, which consist of iodinated arylic compounds, reach densities of 1.6 g/cm3 and have low intrinsic viscosities. Poliovirus, Newcastle disease virus, and lymphocytic choriomeningitis virus were centrifuged to equilibrium in gradients made of these substances. Viral infectivities were not measurably affected, which is especially noteworthy in the case of the very labile lymphocytic choriomeningitis virus. Buoyant densities were found to be significantly lower than densities obtained with gradients made of CsCl and sucrose.

Centrifugation, Density Gradient↗
PubMed1975

High resolution investigations with the scanning and transmission electron microscope of haemadsorption binding sites of mumps virus-infected HeLa cells.

Specific changes at the surface of HeLa cells infected with mumps virus were investigated in parallel with the scanning and transmission electron microscope. The distribution of haemadsorption binding sites and virus-induced antigens at cell surfaces was simultaneously studied by labelling virus-specific antigens with peroxidase-conjugated antibodies after haemadsorption. New information was obtained upon the three-dimensional aspect of the red blood cells, the topographical distribution of their binding sites on the infected cells, and the specific structures at the cell surface which are involved in the process of haemadsorption.

Animals↗