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Biomedical subjects

R Rott

Publications and source records attributed to R Rott.

At least 163 records · Page 9Linked to original sources
PubMed1980

Genetic relatedness of the neuramindase of influenza A strains Nav2, Nav3, and Nav6.

By molecular hybridization and by neuraminidase inhibition tests it is shown that all influenza A strains tested carrying an Nav3 or Nav2 neuraminidase (NA) are genetically highly related in their NA genes and cross-react serologically with specific antineuraminidase sera. The Nav6 strains exhibit a very low RNase protection after hybridization and do not cross-react serologically with Nav2 or Nav3 strains. Thus, the Nav2 and Nav3 strains comprise one group which is distinct from that of Nav6 strains.

Cross Reactions↗
PubMed1980

Cleavability of hemagglutinin determines spread of avian influenza viruses in the chorioallantoic membrane of chicken embryo.

The spread of infection in the chorioallantoic membrane (CAM) has been analysed with pathogenic and non-pathogenic avian influenza A viruses. After allantoic inoculation of pathogenic strains, high titers of infectious virus were found in the allantoic fluid, and virus growth could be demonstrated by immunohistology and electron microscopy in the allantoic epithelium, the mesenchyma, and in the chorionic epithelium. By the same route of inoculation, non-pathogenic strains yielded also higher titers of infectious virus in the allantoic fluid, but virus replication was restricted to the allantoic epithelium and did not occur in the other cell layers. After chorionic inoculation of pathogenic strains, replication occurred in all layers of the CAM, and infectious virus was released into the allantoic fluid. However, when the chorionic epithelium was infected with a non-pathogenic strain, infection did not spread beyond the site of inoculation. These differences in virus spread are based on differential activation of the hemagglutinin by proteolytic cleavage. The hemagglutinin of pathogenic strains is cleaved in cells of each layer, whereas the hemagglutinin of non-pathogenic strains is cleaved only in the allantoic epithelium. In epithelial cells, virus budding occurred nearly exclusively at the apical side of the cell surface, but this polarization of virus maturation was found with both pathogenic and nonpathogenic strains, indicating that it does not account for the differences in virus spread and, thus, in pathogenicity.

Allantois↗
PubMed1980

Replication of Borna disease virus in cell cultures.

Borna disease (BD) virus from infected brain tissue of horses or rabbits could be grown in embryonic brain cells from rabbits or rats with high virus yields. The cells became persistently infected and could be subcultivated without loss of infectivity. Cocultivation of infected rabbit brain (ERB) cells with GMK-, Vero-, or MDCK-cells led to persistently infected cell lines. BD virus grown in MDCK cells after cocultivation became adapted to this cell type and could be used directly for further infection of MDCK cells.

Animals↗
PubMed1980

Mutational changes of the protease susceptibility of glycoprotein F of Newcastle disease virus: effects on pathogenicity.

Two chemically induced mutants with an alteration in the susceptibility of glycoprotein F to proteolytic cleavage have been isolated from the apathogenic strains of La Sota and Ulster of Newcastle disease virus. In contrast to the La Sota wild type, cleavage of the precursor F0 and activation of cell fusing activity and infectivity take place if the mutant is grown in MDBK and BHK21-F cells. The mutant is, therefore, able to undergo multiple replication cycles in cells non-permissive for the wild type. This increase in host range is paralleled by an increase in pathogenicity for chick embryos. The increase in host range of the Ulster mutant is less distinct. This mutant, which does not differ in pathogenicity from its wild type, produces in MDBK cells incompletely activated virus containing predominantly glycoprotein HN in the uncleaved and glycoprotein F in the cleaved form. The data support the concept that the susceptibility of the virus glycoproteins to proteolytic activation is an important factor in determining the pathogenicity of this virus.

Animals↗
PubMed1979

The effect of antibiotics on the photocycle and protoncycle of purple membrane suspensions.

The interrelation was studied between the phototransient absorbing maximally at 412 nm (M412) and light-induced proton release under steady-state conditions in aqueous suspensions of 'purple membrane' derived from Halobacterium halobium. The decay of M412 was slowed down by the simultaneous application of the ionophoric antibiotics valinomycin and beauvericin. The former had only slight activity alone and the latter was effective only in conjunction with valinomycin. The steady-state concentration of M412 which was formed on illumination was a direct function of the concentration of valinomycin. Maximum stabilization of M412 was obtained when the valinomycin was approximately equimolar with the bacteriorhodopsin. Addition of salts to the medium increased the number of protons released per molecule of M412 without affecting the level of M412 which was produced by continuous illumination. The effectiveness of the salts in this respect depended on the nature of the cation. Ca2+ and their antagonists La3+ and ruthenium red were found to have especially high affinity for the system. The extent of light-induced acidification could not be enhanced by increasing the pH of the medium from 6.5 to 7.8. The possible mechanism of action of the ionophores and of the cations on the photocycle and on the proton cycle is discussed.

Anti-Bacterial Agents↗
PubMed1979

Influenza virus-specific T cell-mediated cytotoxicity: integration of the virus antigen into the target cell membrane is essential for target cell formation.

This study deals with the requirements for target cell recognition by influenza A virus-specific cytotoxic T lymphocytes (CTL). H-2-identical cells were incubated with infectious or UV light-inactivated influenza A virus expressing either cleaved or uncleaved hemagglutinin (HA). Thereafter, the treated cells were tested in a 4-h 51Cr assay for susceptibility to CTL-mediated cytolysis. Regardless whether the influenza virus was infectious, virions expressing cleaved HA were efficient in target cell formation. In contrast, cells incubated with either active or UV-inactivated virions expressing uncleaved HA were not lysed by virus-specific CTL. Yet, after mere trypsin-mediated cleavage of the HA of cell-absorbed viroins, strong cytolysis could be observed. On the other hand, solubilization of the envelope lipid bilayer by ethylether abolished the capacity of the remaining HA to induce target cell formation. The results clearly suggest that mere absorption of virions to the membrane of cells, which is performed by virus with uncleaved HA, is insufficient for target cell formation. For this, both cleaved HA and an intact envelope appear to be crucial. We conclude that fusion of the virion into the cell membrane is essential for target cell formation.

Antigens, Surface↗
PubMed1979

Spread of infectious virus along the optic nerve into the retina in Borna disease virus-infected rabbits.

Selective damage of the optic nerve of 14 rabbits without interfering with the choroidal blood flow which supplies the retina and without altering the autonomic nerve supply was successfully achieved by Xenon coagulation. This procedure interrupted the axonal pathway between the brain and the eye. After experimental infection with Borna disease virus the typical disease could be induced. The pathognomonic retinopathy as well as characteristic perivascular choroidal infiltrates, however, did not appear in eyes with coagulated nerve heads. In general virus-specific antigen or infectious virus were not present in the retinas of such damaged eyes. These results permit the conclusion that the ocular expression of Borna disease is a consequence of virus transport via the optic nerve.

Animals↗
PubMed1979

Characterization of virus-like particles produced by an influenza A virus.

The influenza strain 413 1,1 segregated as a stable recombinant during passage of the isolate 19/N which was obtained after double infection of chick embryo fibroblasts by virus N and the fowl plague virus (FPV) mutant ts 19. Its gene constellation was determined by molecular hybridization. Upon infection of chick embryo cells by this recombinant strain, two particle populations of high (H) and low (L) buoyant densities were produced. By biological and biochemical parameters, the H-population (delta = 1.22 g/cm3) cannot be distinguished from standard infectious influenza virus. In contrast, the noninfectious L-particles (delta = 1.14 g/cm3) lack all virus-specific glycoproteins (HA, NA) as well as the matrix protein M and are visualized by electron microscopy as spikeless particles. Significant changes in the quantitative composition of the phospholipid bilayer are evident as compared to the H-particles. In addition to the previously characterized eight genes both populations contain a variety of smaller RNA fragments which hybridize with complementary RNA and presumably represent degradation products of full-length genes.

Animals↗
PubMed1979

The M protein of influenza viruses has no immunizing effect.

Influenza A virus M protein was prepared by electrophoresis in SDS polyacrylamide gel from virus particles which had been pretreated with octylglucoside to remove the surface glycoproteins; M antigens from the influenza virus strains A/Victoria/3/75 (H3N2), A/FPV/Rostock (Hav1N1) and A/chick/Germany/49 (Hav2Neq1) did not protect mice against a lethal challenge infection with the virulent Victoria strain.

Animals↗
PubMed1979

Correlation of pathogenicity and gene constellation of influenza A viruses. III. Non-pathogenic recombinants derived from highly pathogenic parent strains.

We have demonstrated by recombination of two highly pathogenic avian influenza viruses [A/FPV/Rostock (Hav1N1) x A/turkey/England/63 (Hav1Nav3)] that recombinants can be isolated which are pathogenic as well as non-pathogenic for chickens. They carried the glycoproteins of either parent strains, and all are produced in infectious form in chick embryo cells. Genetic analysis revealed that the non-pathogenic recombinants possess a mixed RNA polymerase complex, consisting of pol 1, pol 2, ptra and NP gene products, while, with one exception, the pathogenic recombinants have the genes coding for the polymerase activity from one or other parent virus. The biological properties of the recombinant viruses did not correlate with their pathogenicity for chickens.

Animals↗
PubMed1979

The spread of a pathogenic and an apathogenic strain of Newcastle disease virus in the chick embryo as depending on the protease sensitivity of the virus glycoproteins.

The pathogenic strain Italien and the apathogenic strain Ulster of Newcastle disease virus have been compared with respect to organ tropism and spread of infection in 11-day-old chick embryos. After infection of the endodermal layer of the chorioallantoic membrane by intra-allantoic inoculation with strain Italien, high virus titres are found in all extra-embryonic membranes and fluids and in the embryo itself. Infection results in early death of the embryo. In contrast, after infection with strain Ulster by the same route of inoculation, high virus titres are found only in the allantoic sac and embryos are not killed. Inoculations with strain Italien on to the ectodermal layer through an artificial air sac results in rapid spread of infection in the chorioallantoic membrane and the embryo dies before the virus invades other tissues including the embryo. Under the same conditions of infection, strain Ulster neither spreads within chorioallantoic membrane nor does it kill the embryo. Virus spread in each germinal layer of the chorioallantoic membrane was analysed by immune fluorescence. These studies showed that endoderm as well as mesoderm and ectoderm allowed the spread of strain Italien, whereas only the endoderm is permissive for strain Ulster. These differences in host range are based upon differential activation of the virus glycoproteins by proteolytic cleavage. The glycoproteins of strain Italien are cleaved in each germinal layer, whereas those of strain Ulster are cleaved only in endoderm. These studies demonstrate that, in the system analysed here, spread of infection and organ tropism are important factors for pathogenicity and both of these factors are determined by the susceptibility of the virus glycoproteins to proteolytic cleavage.

Allantois↗