Participation of Deoxyribonucleic Acid in the Multiplication of Influenza Virus

Barry, Richard D.; Ives, Daniel; Cruickshank, J.G.

doi:10.1038/1941139a0

Cited by 151 publications

(39 citation statements)

References 12 publications

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“…The production of fowl plague virus and the PR 8 strain were not completely inhibited and in other experiments we frequently found that inhibition of the Asian strain was not complete. This effect is different from that found with inhibitors of DNA function such as actinomycin D, where the degree of inhibition varies directly with the dose of inhibitor and where virus production can be completely inhibited (Barry, Ives & Cruickshank, 1962). …”

Section: Degree Of Inhibitioncontrasting

confidence: 83%

The effects of UK 2054 on the multiplication of influenza viruses

Barry

Davies

1970

J. Hyg.

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SummaryThe isoquinoline compound UK 2054 prevents the uptake of influenza virus by susceptible cells. Pre-incubation of virus particles with 500μg./ml. UK 2054 at 37°C. for 2 hr. does not reduce virus infectivity. Host cells vary in their responsiveness to the inhibitory effect of UK 2054; virus multiplication is inhibited in chick allantoic cells by lower concentrations than those required to inhibit virus growth in chick embryo fibroblasts. The effectiveness of UK 2054 is reduced by the presence of serum.It is concluded that inhibition of influenza virus multiplication by UK2054 might result from interaction of the inhibitor with both virus and cells. Any direct combination between inhibitor and virus is completely reversible.

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Section: Degree Of Inhibitioncontrasting

confidence: 83%

The effects of UK 2054 on the multiplication of influenza viruses

Barry

Davies

1970

J. Hyg.

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“…This can be interpreted as indicating that the replication of A/WSN is interfered with at the level of primary transcription or at an earlier step. Actinomycin D (1 p~g/ml), which inhibits the transcription of the influenza virus genome (Barry et al, 1962;Scholtissek & Rott, 1970;Ports, 1973), was added to the cultures 30 rain before the removal of cycloheximide to inhibit secondary transcription, but this treatment had little effect on viral protein synthesis (data not shown), indicating that the viral proteins synthesized under the above conditions are the translation products of the primary transcripts. A/WSN ts-65 has no capacity to initiate primary transcription at the non-permissive temperature (39.5 °C), while ts-53 fails to induce v R N A synthesis subsequent to primary transcription at 39 -5 °C (Sugiura et al, 1975 ;Krug et al, 1975).…”

Section: Interference Occurs At the Level Of Primary Transcriptionmentioning

confidence: 99%

Mechanism of Interference Between Influenza A/WSN and B/Kanagawa Viruses

Aoki

Nishiyama

Tsurumi

et al. 1984

Journal of General Virology

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SUMMARYSimultaneous infection of MDCK cells with influenza viruses A/WSN and B/Kanagawa resulted in mutual interference with virus protein synthesis and in significant suppression of A/WSN growth. When infection by one virus preceded the other by 1 or 2 h, growth of the superinfecting virus was selectively inhibited at the level of transcription. Interference by the pre-infecting virus was strongly dependent on the expression of the viral genome but not on haemagglutinin activity. When the replication of both virus types was restricted to primary transcription by cycloheximide, the only translation products following removal of the drug were those of the preinfecting virus. This result was not affected by blocking secondary transcription by actinomycin D. These findings suggest that intertypic interference occurs at the level of primary transcription. This concept was supported further by the observation that a ts mutant of A/WSN (ts-65) with a defect in primary transcription interfered only with superinfection by B/Kanagawa at the permissive temperature.

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“…For example, three types of transcription initiation are known: i) de novo initiation by vesicular stomatitis virus RNA polymerase (1,2); ii) RNA-primed initiation by influenza virus RNA polymerase (3,4); and iii) protein-primed initiation by polio virus RNA polymerase (5,6). Of these three initiation types, the RNA-primed initiation depends most on host cell functions, because it requires a constant supply of host cell mRNA (7,8).…”

Section: Introductionmentioning

confidence: 99%

RNA polymerase of influenza virus. IV. Catalytic properties of the capped RNA endonuclease associated with the RNA polymerase

Kawakami¹,

Mizumoto²,

Ishihama³

1983

Nucl Acids Res

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Catalytic properties of the capped RNA-specific endonuclease associated with the influenza virus RNA polymerase were analyzed with use of synthetic hetero-and homopolymers containing 32P-labeled CAP structures at their 5' termini. The endonuclease displays its intrinsic activity provided that substrate RNA contains both the CAP-1 structure (m7GpppGm) and either A or U residues at 9 to 11 nucleotides distant from the CAP structure. Independent recognition of multiple RNA signals by the endonuclease was further supported by the findings that dinucleotide ApG, free CAP structures and RNA without the CAP structure inhibited the endonuclease activity to different extents.

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Participation of Deoxyribonucleic Acid in the Multiplication of Influenza Virus

Cited by 151 publications

References 12 publications

The effects of UK 2054 on the multiplication of influenza viruses

The effects of UK 2054 on the multiplication of influenza viruses

Mechanism of Interference Between Influenza A/WSN and B/Kanagawa Viruses

RNA polymerase of influenza virus. IV. Catalytic properties of the capped RNA endonuclease associated with the RNA polymerase

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