- Volume 9, Issue 2, 1970
Volume 9, Issue 2, 1970
- Articles
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Virus Group Meeting
The Virus Group of the Society for General Microbiology will meet at the Middlesex Hospital Medical School on 5 and 6 January 1971. The first day will be a symposium on ‘Virus-induced changes in host cells’, with the following invited speakers:
Dr P. Helena Makela, Central Public Health Laboratory, Helsinki. ‘Phage-induced thanges in host cell surface structure.’
Dr D. A. McCarthy, Queen Mary College, London. ‘Virus-induced changes in plant cells.’
Dr I. A. Macpherson, Imperial Cancer Research Fund, London. ‘Transformation of animal cells by tumour viruses.’
Dr J. D. Pitts, Department of Biochemistry, University of Glasgow. ‘Enzyme induction by DNA-containing animal viruses.’
Dr H. Schulte-Holthausen, Würzburg, Germany. ‘Epstein—Barr virus DNA in Burkit tumour cells.’
Chairman—Dr H. G. Pereira
6 January will be a day of contributed papers related to the theme of the symposium.
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Interference with Cell Viability and Poliovirus Multiplication by Polyinosinic-Polycytidylic Acid
More LessSUMMARYThe double-stranded complex of polyinosinic and polycytidylic acids (poly I:C) inhibits the replication of poliovirus in Detroit cells. By a plaque reduction assay a linear relationship was found between the logarithm of the plaque reduction % and the logarithm of the poly I:C concentration, with about 50% inhibition by 0.1 µg./ml. of poly I:C.
The maximum hypochromic effect at 233 nm. on complexing of the polynucleotides occurred with 6 volumes of poly I and 4 volumes of poly C from equimolar solutions of the two homopolynucleotides. Gel-filtration of such a complex on Sepharose 4 B separated double and single strands. Of the added poly I 7% remained as single strands at the conditions of maximum hypochromic effect.
The poly C was found to have a chain length several times larger than that of poly I.
Cell multiplication proceeded at normal rate for 48 hr in a spinner culture with 5 µg./ml. of poly I:C. With 25 µg./ml. no cell multiplication took place within 3 days, and 65% of the cells were dead, whereas in a control culture the cell density doubled and only 15% of cells were dead.
Isolation of RNA from the cells 3 hr after addition of the inducer showed about 20% higher incorporation of [14C]uridine-2 into the treated cells. The increase of incorporation was evenly distributed in all RNA bands except for the 32 s RNA band which contained about 60% more 14C than the 32 s RNA of the control.
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Serological Relationship of Strains of Tobacco Necrosis Virus and their Ability to Activate Strains of Satellite Virus
More LessSUMMARYAntisera prepared in rabbits against strains of tobacco necrosis virus (TNV) or satellite virus (SV) were most specific in precipitation tube tests when animals were bled after single intravenous injections. In Ouchterlony tests, antisera remained equally specific after further injections, including one intramuscular injection. However, all antisera and both test methods agreed in placing the eight strains of TNV tested in two distinctive groups or serotypes. The three strains of SV tested differed as much antigenically from one another as did strains of the two serotypes of TNV, although SV1 and SVc were more closely related to each other than to SV2.
Some strains of TNV aid the multiplication of SV1 and SV2 but not of SVc; others aid SVc but not SV1 or SV2. The ability of different strains of TNV to aid the multiplication of the three strains of SV is correlated with their ability to infect tobacco and bean plants, but not their serological relationship.
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Sensitivity to Inactivation by Ultraviolet Light of Certain Functions of Polyoma Virus: Cell Surface Antigen
More LessSUMMARYUltraviolet irradiation of polyoma virus inactivates different functions of the virus genome. This inactivation is related to the radiation dose.
It has been shown that the ultraviolet radiation target size of the nuclear T antigen is one-half that of the ability to form plaques, and that the radiation target size of the homograft rejection antigen is one-sixth that of the latter. In the present experiments, ultraviolet irradiation has been applied in a similar manner in order to study the cell surface antigen. Quantitative analysis shows that the radiation target size for this antigen is one-half that of the ability to form plaques (infectivity).
The difference in responses of the cell surface antigen and in the homograft rejection antigen observed after irradiation of the virus can be due either to differences in sensitivities of the techniques used or to a difference in antigenicity. Experiments with defective polyoma strains favour a difference in antigenicity.
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Synthesis of Virus Macromolecules in L-929 Cells Infected with Mayaro Virus
More LessSUMMARYTwo electrophoretically distinct protein subunits were found in Mayaro virus, a group A arbovirus. In addition, the cytoplasm of L-929 cells infected with Mayaro virus contained five new proteins, two of which were identified as virus structural proteins. All five new proteins were present by 3 hr after infection. The slower migrating virus structural protein stimulated the production of virus-neutralizing antibody.
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Effect of Interferon on the Replication of Sendai Virus
More LessSUMMARYThe incorporation of [3H]uridine into the four species of RNA specified by Sendai virus in monolayers of chick embryo fibroblasts was inhibited to an equal degree by addition of purified chick interferon to cultures before infection with virus. The inhibition of RNA synthesis was dose-dependent. Similarly, [3H]uridine incorporation into RNA of virus nucleocapsid and polyribosomes was completely inhibited by pretreatment with interferon. When interferon was added 2 hr after infection, there were only small effects on the synthesis of total virus-specific RNA and significantly greater reduction was observed in [3H]uridine incorporation into the RNA of nucleocapsid and polyribosomes. Although Sendai infection does not interfere with host-cell protein or RNA synthesis, interferon added 6 hr or later after infection did not affect any Sendai replicative functions.
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Volume 5 (1969)
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Volume 4 (1969)
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Volume 3 (1968)
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Volume 2 (1968)
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Volume 1 (1967)