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R Rott

Publications and source records attributed to R Rott.

At least 145 records · Page 8Linked to original sources
PubMed1982

The overall evolution of the H7 influenza virus haemagglutinins is different from the evolution of the proteolytic cleavage site.

It has been shown previously that the pathogenicity of avian influenza A viruses depends strictly on the proteolytic cleavability of their haemagglutinins (HAs) in infected cells. In this communication, pathogenic and non-pathogenic strains of the H7 subtype have been studied by comparing the genetic relatedness of their HA genes. Some of the cleavable HAs of pathogenic strains were genetically more closely related to the uncleaved HAs than to other cleavable HAs. These data clearly demonstrate that the overall evolution of the H7 haemagglutinins is different from the evolution of the specific cleavage site.

Biological Evolution↗
PubMed1982

The specificity of viral sialidases. The use of oligosaccharide substrates to probe enzymic characteristics and strain-specific differences.

1. The action of sialidases from Newcastle disease virus (NDV), influenza A2 virus (IA2V) and fowl plague virus (FPV) on sialyloligosaccharide substrates containing alpha 2-3, alpha 2-6 or alpha 2-8 linkages was studied. 2. In all cases 2-3-linked sialic acids were preferentially released. Compared with II6Neu5AcLac, all 2-6-linked substrates, including sialyl-N-acetyllactosamine and its asparaginyl derivative, a urinary hexasaccharide and Neu5Ac(2-6)GalNAc were cleaved at improved rates by NDV and less by FPV sialidases. In the case of IA2V sialidase the asparaginyl oligosaccharide was very poorly cleaved, illustrating a variation in viral strain specificity. 3. A decrease in relative rates was observed in the order NDV greater than IA2V greater than FPV for substrates with 2-3 linkages relative to II6Neu5AcLac. The greatest relative rate was 470-fold higher. The 2-3-linked sialyl-N-acetyllactosaminylasparagine and IV3Neu5AcLcOse4 were poor substrates for the IA2V sialidase, but the rates were greater than with the 2-6 linked substrates. 4. The ganglioside substrate II3Neu5AcLacCer showed lower activity than its oligosaccharide analogue, but neither II3Neu5AcGgOse4Cer nor its oligosaccharide were substrates. 5. The Km values for 2-6-linked substrates were generally of the order 10 mM while those for the 2-3-linked substrates were approximately 1 mM. The V values were consistently higher for the 2-3-linked substrates. IV3Neu5AcLcOse4 showed high Km and very high V values, while the 2-8-linked disialyllactose showed this trend only with NDV enzyme, the IA2V and FPV sialidases exhibiting high Km and low V values. 6. The results are discussed in the light of the current knowledge of viral sialidase specificity and relative to the binding of virus particles to cell surfaces.

Colorimetry↗
PubMed1981

Purification and immunological properties of proton-ATPase complexes from yeast and rat liver mitochondria.

Proton-ATPase complexes from yeast and rat liver mitochondria were isolated by a simple method previously employed for the purification of the proton-ATPase complex from chloroplasts. After reconstitution into liposomes, the purified complexes were active in the ATP-Pi exchange reaction, the rate of which was 120 and at least 200 nmol/mg of protein/min for the rat liver and yeast mitochondria ATPases, respectively. Upon sodium dodecyl sulfate polyacrylamide gel electrophoresis, each complex exhibited 11 to 12 different polypeptides. The isolated ATPase complexes from rat liver and yeast mitochondria, from Swiss chard chloroplasts, and Escherichia coli membranes were reacted with antibodies prepared against the various subunits of ATPase complexes. From all the combinations of antigen-antibody examined, only the antibodies against beta subunit cross-reacted with the corresponding subunit of all the ATPase complexes tested. These results indicate that certain amino acid sequences in the beta subunit have been preserved in all of the proton-ATPase complexes.

Adenosine Triphosphatases↗
PubMed1981

The site of cleavage in infected cells and polypeptides of representative paramyxoviruses grown in cultured cells of the chorioallantoic membrane.

Cultured cells of the chorioallantoic membrane (CAM) fulfilled the need of using the same cell system that was permissive for representative paramyxoviruses to carry out studies on the biosynthesis of their glycoproteins in infected cells. The polypeptides composition of the respective paramyxoviruses [Newcastle disease virus (NDV), paramyxovirus Yucaipa (PMY), and Sendai virus], grown in eggs and CAM-cells, was essentially identical. In egg-grown PMY a large glycoprotein (LGP) was present but only in some CAM-grown preparations of virus labeled with [3H]-glucosamine and rarely in [35S]-methionine or [3H]-amino acids (valine, leucine, and tyrosine) labeled viruses. The site of cleavage of precursor F0 to F1,2 was not the same. In contrast to the cleavage of Sendai virus glycoprotein, cleavage was intracellular in NDV and PMY infected cells. Homologous antisera against the glycoproteins failed to inhibit cleavage of HN0 or F0 in cells infected with the representative paramyxoviruses.

Allantois↗
PubMed1981

Intrinsic interference between swine influenza and fowl plague virus.

Multiplication of swine influenza (SW) virus is inhibited by fowl plaque virus (FPV) at the level of RNA synthesis when host cells are infected with both viruses at a high multiplicity of infection. Under these conditions reassortment between the two viruses cannot be detected. The inhibitory effect of FPV is highly reduced and recombinants between the two viruses could be obtained when the cells were superinfected with FPV 1--2 hours after infection with SW virus, or after simultaneous infection with a low multiplicity of infection. The phenomenon is compatible with the intrinsic interference.

Animals↗
PubMed1981

Productive infection of chick embryo cells by influenza viruses tightly bound on substratum.

To test whether penetration of influenza viruses could occur at the plasma membrane of host cells, virus particles were tightly bound on Concanavalin A-coated substratum of plastic culture plates and then overlayed with embryo cells. Under these conditions, endocytosis of the viruses was prevented but the cells were found to be effectively infected. The results indicate, that infection by influenza viruses can occur through fusion between the viral membrane and the host cell plasma membrane.

Animals↗
PubMed1981

Reactivity of antibodies in human serum with antigens of an enteropathogenic bovine coronavirus.

Antibodies in human serum against an enteropathogenic bovine coronavirus were detected by double immunodiffusion (DID), neutralization of infectivity, indirect immunofluorescence, and immune electron microscopy. Human sera reacting in the DID test neutralized the infectivity of the bovine coronaviruses to indices of 2.5 to greater than 5. Nineteen of 40 DID-negative, heat-inactivated sera had neutralizing indices of 1 to 3.0. Human serum with neutralizing and DID antibodies produced juxtanuclear and cytoplasmic fluorescence identical to that of bovine immune serum in cells infected with the bovine coronavirus. Antibodies in human and bovine sera interacted with the peplomeres of the bovine coronavirus, matting and bridging them, when present in excess, and facilitated formation of large viral aggregates when present in equivalent concentrations. Complement added to the virus-antibody complexes did not alter specifically the morphology of single, antibody-laden viral particles or viral particles in aggregates. Evidence of the transmission of coronavirus from experimentally inoculated calves to man, with ensuing gastroenteritis, was found by electron microscopic tracing of the coronavirus and its virus-antibody complexes.

Animals↗
PubMed1981

Enhancement of plaque formation and cell fusion of an enteropathogenic coronavirus by trypsin treatment.

Plaque formation, replication, and related cytopathic functions of the enteropathogenic bovine coronavirus strain L9 in bovine fetal thyroid (BFTy) and bovine fetal brain (BFB) cells were investigated in the presence and absence of trypsin. Plaque formation was enhanced in both cell types. Plaques reached a size with an average diameter of 5 mm within 4 days with trypsin in the overlay, whereas their diameter remained less than 1 mm at this time after plating without trypsin in the overlay. Fusion of both cell types was observed 12 to 18 h after infection when trypsin was present in the medium. Fusion was not observed in infected BFB cell cultures and was rarely observed 48 h after infection of BFTy cells maintained with the trypsin-free medium. The largest polycaryons formed had 15 to 22 nuclei. They then lysed and detached. Cell fusion depended on de novo synthesis of hemagglutinin and infectivity. Fusion from without was not observed. Virus produced under trypsin-enhancing conditions accompanied by cell fusion did not lyse mouse erythrocytes that reacted with L9 coronavirus hemagglutinin. Trypsin-treated, infected BFTy cultures produced coronaviral particles that excluded stain from the envelope confinement. These virions had uniformly shorter surface projections than did the viral forms generated by trypsin-free cell cultures.

Animals↗
PubMed1980

Genetic determinants for infectivity and pathogenicity of influenza viruses.

The objective of the studies presented was to define a molecular basis for infectivity and pathogenicity of influenza virus. It is demonstrated that activation of the HA glycoprotein by post-translational proteolytic cleavage is indispensable for the formation of infectious influenza virus. There are two preconditions for influenza virus to be pathogenic: (1) the presence on the virus particle of a cleaved HA molecule essential for the infectivity, and (2) an optimal genome composition. In naturally occurring avian influenza viruses there is a direct correlation between the cleavability of the haemagglutinin, the potential of the virus to be produced in infectious form in a wide range of host cells, and the viruses' pathogenicity for chicken. It is concluded that Nature selects an optimal gene constellation for each individual field strain. In these viruses the structure of the haemagglutinin is the determining factor for pathogenicity.

Animals↗