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Biomedical subjects

R Rott

Publications and source records attributed to R Rott.

At least 199 records · Page 11Linked to original sources
PubMed1976

Attenuation of pathogenicity of fowl plague virus by recombination with other influenza A viruses nonpathogenic for fowl: nonexculsive dependence of pathogenicity on hemagglutinin and neuraminidase of the virus.

A number of antigenic hybrids of influenza A viruses were produced possessing either the hemagglutinin or the neuraminidase of fowl plague virus and the corresponding antigen derived from another influenza A virus. Other recombinants were obtained carrying both surface antigens of fowl plague virus but differing from the parent in certain biological properties. None of the recombinants isolated were pathogenic for adult chickens. Most recombinants obtained after crosses between reciprocal recombinants carrying both fowl plague virus surface antigens were also apathogenic for chickens. Using the same parent recombinants for double infection some of the progeny "back-recombinants" were pathogenic, whereas others were not. From these results it is concluded that the surface components do not by themselves determine the pathogenicity of influenza A viruses.

Animals↗
PubMed1975

Antigenic relationship between the surface antigens of avian and equine influenze viruses.

Influenza virus Equine 1 (A/equine/Prague/56) has a hemagglutinin which is antigenically related to the hemagglutinin of fowl plague virus strain Rostock (FPV) and a neuraminidase which cross-reacts with the enzyme of virus N (A/chick/Germany/49). After a single injection of chickens with Equine 1 virus no hemagglutination inhibiting (HI) and neutralizing antibodies against FPV can be demonstrated, although the birds are fully protected against a lethal dose of FPV. HI and neutralizing antibodies against FPV appear after a second injection of Equine 1 virus several weeks after the first one. Liberation of newly sunthesized FPV from the host cell is ingibited by antibodies cross-reacting with any antigen of virus surface.

Animals↗
PubMed1975

Effect of tetraethyl thiuram disulfide (disulfiram) on the multiplication of enveloped viruses.

Disulfiram at concentrations between 0.1 and 0.3 mM inhibits the multiplication of Semliki Forest virus (SFV), fowl plague virus (FPV), Newcastle disease virus (NDV), vesicular stomatitis virus (VSV), and pseudorabies virus (PRV), when administered 1 hour before and during adsorption. There is, however, no inhibition of virus multiplication, when the drug is added after adsorption onto chick embryo cells. Disulfiram interferes neither with the receptors of the virus nor of erythrocytes, and it does not prevent virus adsorption. Possibly an early step in virus multiplication is affected by disculfiram. Infected cells once treated with the drug recover after some time of incubation in an ingibitor-free medium. The inhibitory state can be maintained, however, if relatively low doses of disulfiram are present in the culture medium also after adsorption. Disulfiram has no effect on macromolecular synthesis of the host cells. It has, however, a marked affect on membrane function. While virus multiplication is readily inhibited by disulfiram when chick embryo or BHK cells were investigated, virus multiplication in HeLa cells is almost resestant against the action of disulfiram.

Adsorption↗
PubMed1975

Effect of 2-deoxy-D-glucose on herpesvirus-induced inhibition of cellular DNA synthesis.

In pseudorabies virus-infected cells host DNA synthesis is turned off 4 to 5 h postinfection. In the presence of 0.5 mM 2-deoxy-D-glucose, however, synthesis of both cellular and viral DNA proceeds unimpaired throughout the virus replication cycle. The uptake of radioactive thymidine into mock-infected cells is not altered in the presence of 2-deoxy-D-glucose. Virus-specific protein synthesis and particle formation also proceed in medium containing the deoxy sugar, but the virus particles produced are noninfectious and cell fusion is inhibited.

Animals↗
PubMed1975

Inhibition of cellular protein synthesis by simultaneous pretreatment of host cells with fowl plague virus and actinomycin D: a method for studying early protein synthesis of several RNA viruses.

A method is described for analysis of viral protein synthesis early after infection when minute amounts of viral proteins are effectively concealed by large amounts of produced host-specific proteins. The method is superior to a radioimmune assay, since all virus-induced proteins can be measured independent of their immunological reactivity. Host-specific protein synthesis can be suppressed by infection with fowl plague virus. Addition of actinomycin C 1.25 h postinfection does not prevent this suppression, but it does block effectively the formation of fowl plague virus-specific proteins. Such cells synthesize only small amounts of cellular proteins, as revealed by polyacrylamide electrophoresis. They can be superinfected with several different enveloped viruses, however, without significant diminution of virus yeilds. In pretreated cells the eclipse is shortened for Semliki Forest virus, Sindbis virus, and vesicular stomatitis virus, but prolonged for Newcastle disease virus. The onset of protein synthesis, specific for the superinfecting virus, could be clearly demonstrated within 1 h after superinfection. At this time, in cells superinfected with Semliki Forest virus, great amounts of NSP 75 (nonstructural protein; molecular weight, 75 X 10(3)) and reduced amounts of the core protein C could be deomonstrated. The precursor glycoprotein NSP 68 is followed by a new polypeptide, NSP 65: three proteins with molecular weights exceeding 100 X 10(3) were observed which are missing later in the infectious cycle. Similar results were obtained after superinfection with Sindbis virus. The formation of a new polypeptide with a molecular weight of about 80 X 10(3) was detected. After superinfection with vesicular stomatis virus or Newcastle disease virus the formation of new proteins, characteristic for the early stage of infeciton, was not observed.

Cell Line↗
PubMed1974

Inhibition of the multiplication of vesicular stomatitis and Newcastle disease virus by 2-deoxy-d-glucose.

The production of infectious vesicular stomatitis (VSV) and Newcastle disease virus can be completely inhibited by 2-deoxy-d-glucose in pyruvate-containing medium, if virus either grown in pyruvate-containing medium or dialyzed against phosphate-buffered saline is used for infection. Under these conditions, the synthesis of all VSV proteins is reduced. VSV RNA, which is synthesized at reduced rates, seems to be unstable. The effect is completely reversible. If virus grown in glucose-containing medium is used for infection, the production of both viruses is not significantly inhibited by 2-deoxy-d-glucose. Under these conditions the production of the VSV glycoprotein is specifically impaired, but does not lead to a marked reduction of the yield of infectious virus.

Amino Acids↗