The Effects of Substituted Benzimidazoles on the Growth of Viruses and the Nucleic Acid Metabolism of Host Cells

Bucknall, R. A.

doi:10.1099/0022-1317-1-1-89

Cited by 38 publications

(12 citation statements)

References 18 publications

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“…The methods for measuring the effects of aphidicolin and other drugs on the DNA and ribonucleic acid RNA synthesis of tissue culture cells by uptake of 3H-thymidine and 'H-uridine have already been described (2).…”

Section: Methodsmentioning

confidence: 99%

Antiviral Effects of Aphidicolin, a New Antibiotic Produced by Cephalosporium aphidicola

Bucknall¹,

Moores²,

Simms³

et al. 1973

Antimicrob Agents Chemother

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144

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Aphidicolin is an antibiotic of novel structure produced by the mold Cephalosporium aphidicola . It is a potent inhibitor of cellular deoxyribonucleic acid synthesis, and it also strongly inhibits the growth of herpes simplex virus both in tissue culture and in the rabbit eye. Aphidicolin is active against iododeoxyuridine-resistant herpes virus, and does not itself readily induce the formation of drug-resistant strains of herpesvirus.

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Section: Methodsmentioning

confidence: 99%

Antiviral Effects of Aphidicolin, a New Antibiotic Produced by Cephalosporium aphidicola

Bucknall¹,

Moores²,

Simms³

et al. 1973

Antimicrob Agents Chemother

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144

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“…Ribosides of halobenzimidazoles are highly active inhibitors of the multiplication of RNA (3,13,27,29,30) and DNA (16,31,32) viruses and of cellular RNA synthesis (3,14,31). The inhibitory activity of such derivatives increases with multiple substitution of halogen atoms in the benzenoid ring (27,28,29).…”

mentioning

confidence: 99%

Action of dichlorobenzimidazole riboside on RNA synthesis in L-929 and HeLa cells.

Tamm¹,

Hand²,

Caliguiri³

1976

The Journal of Cell Biology

127

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A BSTR ACT 5,6-Dichloro-l-/~-o-ribofuranosylbenzimidazole (DRB) inhibits RNA synthesis in L-929 cells (mouse fibroblast line) and HeLa cells (human epithelioid carcinoma line) within 2 min of addition of the compound to the medium. By removing DRB from the medium, the inhibition is promptly and completely reversed after treatment of cells for as long as I h or even longer. The inhibitory effect of DRB on the overall rate of RNA synthesis is similar in L and HeLa ceils and is markedly concentration-dependent in the low dose range (5-20 #M or 1.6-6.4/~g/ml), but not at higher concentrations of DRB. At a concentration of 12 #M, DRB has a highly selective inhibitory effect on the synthesis of nuclear heterogeneous RNA in L cells. At higher concentrations, there is also inhibition of 45 S ribosomal precursor RNA synthesis, but at all concentrations the effect on heterogeneous RNA synthesis in L cells in considerably greater than that on preribosomal RNA synthesis. In HeLa cells, too, DRB has a selective effect on heterogeneous RNA synthesis, but quantitatively the selectivity of action is somewhat less pronounced. In both L and HeLa cells, the inhibition of synthesis of nuclear heterogeneous RNA is incomplete even at very high concentrations of DRB (150 ~zM). Thus, while DRB is a selective inhibitor of nuclear heterogeneous RNA synthesis, not all such RNA synthesis is sensitive to inhibition. It is proposed that messenger precursor RNA synthesis may largely be sensitive to inhibition by DRB. In short-term experiments, DRB has no effect on protein synthesis in L or HeLa cells. DRB has a slight to moderate inhibitory effect on uridine uptake into L cells and a moderate to marked effect on uptake of uridine into HeLa cells.

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“…DRB also enhances premature termination of SV40 late transcription (Laub et al, 1980). Although it has been shown that DRB and other substituted benzimidazoles inhibit vaccinia virus replication (Tamm & Overman, 1957;Tamm et aL, 1960;Ikegami et al, 1960, Bucknall, 1967, the mechanism of inhibition remains unknown. In view of the apparent requirement of the host nucleus for vaccinia virus replication (Pennington & Follet, 1974;Hruby et al, 1979a, b;Silver et al, 1979) it was decided to investigate the step sensitive to DRB in vaccinia virus replication.…”

Section: Introductionmentioning

confidence: 99%

The Inhibition of Vaccinia Virus Replication by 5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB): an Effect at the Assembly Stage

Pothier

Dru²,

Beaud³

1981

Journal of General Virology

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SUMMARYThe step sensitive to DRB (5,6-dichloro-l-fl-D-ribofuranosylbenzimidazole) in vaccinia virus replication has been investigated. Ninety gM-DRB extensively inhibited the yield of vaccinia virus after infection of Ehrlich ascites tumour cells. DRB did not inhibit cytoplasmic vaccinia DNA replication. Cytoplasmic viral RNA synthesis (both early and late) was also apparently unaffected and the virus RNAs thus synthesized were normal sized. The expression of early, intermediate and late proteins was not detectably impaired by DRB in vaccinia virus-infected cells. DRB inhibited vaccinia virus replication at the assembly stage since most of the virus DNA remained in a DNase-sensitive form in the infected cells and the virus was therefore not normally coated with virus proteins.

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The Effects of Substituted Benzimidazoles on the Growth of Viruses and the Nucleic Acid Metabolism of Host Cells

Cited by 38 publications

References 18 publications

Antiviral Effects of Aphidicolin, a New Antibiotic Produced by Cephalosporium aphidicola

Antiviral Effects of Aphidicolin, a New Antibiotic Produced by Cephalosporium aphidicola

Action of dichlorobenzimidazole riboside on RNA synthesis in L-929 and HeLa cells.

The Inhibition of Vaccinia Virus Replication by 5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB): an Effect at the Assembly Stage

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