Inhibition of herpes simplex virus replication by anthracycline compounds

Ash, Ronald J.; Diekema, Keith A.

doi:10.1016/0166-3542(87)90078-7

Cited by 14 publications

(11 citation statements)

References 6 publications

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“…The drug exhibits broadspectrum antitumor activity and is used for the treatment of cancer, in particular solid tumors (2,13,44,46,50). Doxorubicin was reported to elicit antiviral activity in vitro, including against HIV, herpes simplex virus, Rauscher leukemia virus, and avian myeloblastosis virus (3,21,22,48). On the other hand, however, doxorubicin was reported to cause reactivation of latent viruses, including herpes simplex virus and the Epstein-Barr virus (17,18,54).…”

Section: Discussionmentioning

confidence: 99%

“…Here, we report on the activity against DENV and some other flaviviruses of SA-17, a derivate of the anthracycline antibiotic doxorubicin. The parent compound doxorubicin was earlier shown to be active against a variety of other viruses, such as HIV and herpes simplex virus (3,21,22,48). SA-17 inhibits virus replication by targeting the very early stages of the viral replication cycle.…”

mentioning

confidence: 99%

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A Derivate of the Antibiotic Doxorubicin Is a Selective Inhibitor of Dengue and Yellow Fever Virus Replication In Vitro

Kaptein

Burghgraeve

Froeyen

et al. 2010

Antimicrob Agents Chemother

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

A Derivate of the Antibiotic Doxorubicin Is a Selective Inhibitor of Dengue and Yellow Fever Virus Replication In Vitro

Kaptein

Burghgraeve

Froeyen

et al. 2010

Antimicrob Agents Chemother

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“…and co-ordinately inhibits viral, but not cellular protein synthesis in fowl plague virus-infected BHK-21 cells. Ash and Diekma (1987) have demonstrated that 0.1-0.2ILg mr' concentrations of DMN or ADR depress the virus yields of type 1 and type 2 strains of herpes simplex. Depression of virus yield is attributed to a combination of effects, including direct viral inactivation, inhibition of DNA synthesis, and inhibition of some undefined late event in the replicative cycle.…”

Section: Discussionmentioning

confidence: 97%

“…ADR and DMN have also been shown to inhibit the replication of DNA viruses (DiMarco et al, 1968;Cohen et 131., 1969;Bossa et al, 1975;Minor and Dimmock, 1977;Shortridge and Squires, 1977). However, neither ADR nor DMN is effective against RNA viruses (Ash and Diekma, 1987).…”

Section: Introductionmentioning

confidence: 96%

Enhancement of the Antiviral Activity of Poly (A-U) by Adriamycin and Daunomycin

Jamison

Bonilla

Tsai

1990

Antivir Chem Chemother

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The role of adriamycin (ADR) and daunomycin (DMN) in modulating the antiviral activity of poly (adeylate-uridylate) (poly (A-U)) was examined using a human foreskin fibroblast – vesicular stomatitis virus (HSF-VSV) bioassay in which the concentration of poly (A-U) was fixed at 0.05 mm or 0.2 mm while the ADR or DMN concentration was varied to produce ADR (or DMN)/ribonucleotide ratios ranging from 1:16 to 2:1. Poly (A-U), ADR and DMN were not efficacious antiviral agents when tested individually at the concentrations employed in the ADR (or DMN)/poly (A-U) combinations. When the ADR or DMN was combined with the poly (A-U) to produce ADR (or DMN)/poly (A-U) ratios of 1/6, the 50% effective doses (ED50) of the poly (A-U), ADR and DMN decreased 18, 104, and 185-fold, respectively. However, when ADR or DMN was combined with polyriboinosinic-polyribocytidylic acid [poly (I) · poly (C)], the ED50 of the ADR, DMN and the poly (I) · poly (C) were not affected. Interferon neutralization studies indicated that ADR, DMN, poly (A-U) and the ADR (or DMN)/poly (A-U) combination induced the production of interferon-beta (IFN-β). The amount of IFN produced by the ADR (or DMN)/poly (A-U) combinations was equal to the sum of the IFN prduced by their constituents. These results indicate that the ADR and DMN potentiate the antiviral activity of the poly (A-U) without affecting the amount of IFN induced. The direct viral inactivation study demonstrated that ADR, DMN, poly (A-U) and the ADR (or DMN)/poly (A-U) combinations do not inactivate the VSV at concentrations near the ED50.

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“…Of these, anthracycline compounds inhibit the activity of phospholipase B in a dose-dependent manner [21]. Doxorubicin also inhibits the replication of HIV [22], herpes simplex virus [23], dengue virus, and yellow fever virus [24]. Novel antimicrobial agents might be developed using anthracycline as the lead compound.…”

Section: Discussionmentioning

confidence: 99%

In vitro Synergistic Effects of Anthracycline Antitumor Agents and Fluconazole Against Azole-Resistant Candida albicans Clinical Isolates

S¹

2013

J Dev Drugs

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Inhibition of herpes simplex virus replication by anthracycline compounds

Cited by 14 publications

References 6 publications

A Derivate of the Antibiotic Doxorubicin Is a Selective Inhibitor of Dengue and Yellow Fever Virus Replication In Vitro

A Derivate of the Antibiotic Doxorubicin Is a Selective Inhibitor of Dengue and Yellow Fever Virus Replication In Vitro

Enhancement of the Antiviral Activity of Poly (A-U) by Adriamycin and Daunomycin

In vitro Synergistic Effects of Anthracycline Antitumor Agents and Fluconazole Against Azole-Resistant Candida albicans Clinical Isolates

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