Susceptibility of Herpesviruses to Cytosine Arabinoside: Standardization of Susceptibility Test Procedure and Relative Resistance of Herpes Simplex Type 2 Strains

Fiala, Milan; Chow, Anthony W.; Guze, Lucien B.

doi:10.1128/aac.1.4.354

Cited by 25 publications

(12 citation statements)

References 9 publications

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“…It can be seen that Me-IBT inactivated strains of both type 1 and type 2 HSV, including a strain of HSV type 2 which transforms hamster cells in vitro. The rates of inactivation of the type 1 and 2 strains appear to be quite similar in contrast to previous findings from this laboratory and others (4,6,11,12) with other compounds such as silver nitrate, cytosine arabinoside, and iododeoxyuridine.…”

supporting

confidence: 64%

Inactivation of Herpes Simplex Virus by Thiosemicarbazones and Certain Cations

Levinson

Coleman

Woodson

et al. 1974

Antimicrob Agents Chemother

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supporting

confidence: 64%

Inactivation of Herpes Simplex Virus by Thiosemicarbazones and Certain Cations

Levinson

Coleman

Woodson

et al. 1974

Antimicrob Agents Chemother

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“…5-Iodo-2-deoxyuridine and cytosine arabinoside are two well-known nucleoside analogs and are inhibitors of herpervirus replication. Both compounds are quite toxic (2,12), and 5-iodo-2-deoxyuridine has been shown to be carcinogenic and teratogenic (10).…”

mentioning

confidence: 99%

Inhibition of Herpes Simplex Virus Replication by Phosphonoacetic Acid

Overby

Robishaw

Schleicher

et al. 1974

Antimicrob Agents Chemother

153

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Replication of herpes simplex virus in WI-38 cells was inhibited by phosphonoacetic acid, as measured by decreased virus cytopathogenic effect and incorporation of radiolabeled thymidine in virus-infected cells. The drug appeared to have no effect on adsorption, penetration, or release of the virus nor on the synthesis of ribonucleic acid or protein. It appeared to inhibit virus deoxyribonucleic acid synthesis.Herpes simplex virus (HSV) is a frequent infection in man with degrees of severity from mild to severe discomfort (cutaneous lesions) to severe infection damaging the eye sight (herpes keratitis) to severe and life-threatening diseases (herpes encephalitis). It has been suggested recently that herpes-viruses may be directly or indirectly associated with cancer in several animals: frog renal adenocarcinoma (4), malignant lymphomas in chickens (Marek's disease) (11), rabbits (6), and monkeys (8). Herpes-type viruses have been indirectly associated with Burkitt's lymphoma, nasopharyngeal carcinoma (5), and cervical carcinoma (1) in humans. 5-Iodo-2-deoxyuridine and cytosine arabinoside are two well-known nucleoside analogs and are inhibitors of herpervirus replication. Both compounds are quite toxic (2, 12), and 5-iodo-2-deoxyuridine has been shown to be carcinogenic and teratogenic (10).In earlier studies by Shipkowitz et al. (13), phosphonoacetic acid (PAA) was shown to be active against herpes dermatitis in mice and herpes keratitis in rabbits. We report here the efficacy of PAA against HSV in tissue culture, its effect on WI-38 cells, and studies related to the mechanism of action. Infected cells. Virus stock solutions were diluted in MM and were added to confluent WI-38 cells. The virus was allowed to adsorb for 1 h at 37 C. The medium and unadsorbed virus were removed by decanting and the cells were washed twice with MM. Cell cultures were then incubated at 37 C in MM.Drug tests. PAA was prepared from sodium phosphite and sodium chloroacetic acid as described by Nylen (9). Stock solutions were prepared in MM at a concentration of 10 mg/ml. Portions were then added aseptically to cell cultures to give the desired final concentrations of PAA.Ribonucleic acid (RNA), deoxyribonucleic acid (DNA), and protein synthesis. Cultures (1 ml) of WI-38 cells were grown and infected in tubes. At various intervals during the incubation, the cultures were pulse-labeled for 30 min with [14CIthymidine (0.5 MCi), [3Hjuridine (2.5 1Ci), or "4C-labeled amino acid mixtures (0.2 1Ci). PAA was added at the time of HSV adsorption and was continued in the culture medium thereafter. After each 30-min labeling with radioactive materials, triplicate tubes were removed, and then the medium was decanted. The cell layers were washed twice with cold MM. Then, 4 ml of phosphate-buffered saline were added to each tube, and the cells were scraped from the tube wall. Trichloroacetic acid was added to a final concentration of 5%. The mixture was frozen, thawed once, and

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“…1-f-DArabinofuranosylcytosine (ara-C) has been reported to inhibit both HVH type 1 and type 2 in a variety of cell cultures (5, 10,34) and to be as effective as IUdR in the treatment of experimental HVH keratitis (14,33), and has been used in the treatment of HVH encephalitis in 588 KERN, OVERALL, AND GLASGOW HVH keratitis in hamsters (30) and HVH encephalitis in hamsters and mice (1, 19,29,31,32). Encouraging results have also been reported in the treatment of serious human HVH infections with ara-A (7).…”

mentioning

confidence: 99%

Herpesvirus hominis Infection in Newborn Mice: Comparison of the Therapeutic Efficacy of 1-β- d -Arabinofuranosylcytosine and 9-β- d -Arabinofuranosyladenine

Kern

Overall²,

Glasgow³

1975

Antimicrob Agents Chemother

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Intranasal inoculation of newborn mice with Herpesvirus hominis type 2 provides an experimental infection that closely resembles disseminated herpesvirus infection of human newborn infants. After inoculation of mice, the virus multiplies in the respiratory tract and is disseminated through the blood to the liver and spleen and to the brain by both a viremia and nerve route transmission. Although therapy with 1-β- d -arabinofuranosylcytosine (ara-C) did not reduce final mortality, it did increase the mean survival time by 1 day. This effect on the mean survival time was associated with a 1-day delay in the appearance of herpesvirus in the blood, liver, and spleen and a reduction of virus replication in lung and brain for 1 day as compared with untreated control animals. Treatment with 9-β- d -arabinofuranosyladenine (ara-A) likewise had no effect on final mortality, but increased the mean survival time by 2 days. Therapy with ara-A delayed or suppressed virus replication in blood, lung, liver, spleen, and brain for 2 days. Although treatment with either ara-C or ara-A in this experimental H. hominis type 2 infection resulted in a temporary delay and/or suppression of viral replication in several target organs, neither compound was completely effective in inhibiting viral replication or in protecting animals from eventual death due to the infection.

show abstract

Susceptibility of Herpesviruses to Cytosine Arabinoside: Standardization of Susceptibility Test Procedure and Relative Resistance of Herpes Simplex Type 2 Strains

Cited by 25 publications

References 9 publications

Inactivation of Herpes Simplex Virus by Thiosemicarbazones and Certain Cations

Inactivation of Herpes Simplex Virus by Thiosemicarbazones and Certain Cations

Inhibition of Herpes Simplex Virus Replication by Phosphonoacetic Acid

Herpesvirus hominis Infection in Newborn Mice: Comparison of the Therapeutic Efficacy of 1-β- d -Arabinofuranosylcytosine and 9-β- d -Arabinofuranosyladenine

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