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Biomedical subjects

S Alenius

Publications and source records attributed to S Alenius.

48 records · Page 3Linked to original sources
PubMed1987

Effect of bovine virus diarrhoea virus on pregnancy in the ewe monitored by ultrasound scanning and levels of 15-keto-13,14-dihydro-PGF2 alpha and progesterone.

Fourteen unvaccinated and seronegative ewes were experimentally infected with bovine virus diarrhoea virus around day 60 of pregnancy. Two other groups of pregnant ewes served as control animals. The animals were followed with ultrasound scanning to study the status of the fetus and with frequent blood sampling for analysis of progesterone and 15-keto-13,14-dihydro-PGF2 alpha, two hormones that could reflect the propagation of the infection. The unvaccinated ewes responded to the infection with abortion, resorption of the fetus, mummification or no changes at all. The endocrinological changes reflected in a most adequate way the pathological changes in the uterus. Detailed endocrinological studies can contribute to the understanding of the pathogenesis of some infectious diseases that affect reproduction.

Abortion, Veterinary↗
PubMed1983

Antiherpetic activity and mechanism of action of 9-(4-hydroxybutyl)guanine.

9-(4-Hydroxybutyl)guanine was synthesized and tested for antiherpes activity. In cell cultures, different strains of herpes simplex virus type 1 (HSV-1) and type 2(HSV-2) were inhibited by 50% at 2-14 microM of 9-(4-hydroxybutyl)guanine, while a HSV-1 mutant lacking thymidine kinase (HSV-1 TK-) was resistant. Linear competitive inhibition of purified HSV-1-induced thymidine kinase (TK) with thymidine as a variable substrate was observed for 9-(4-hydroxybutyl)guanine with an apparent Ki value of 2.06 microM while the corresponding Ki value for the cellular TK was greater than 250 microM. By using high performance liquid chromatography, the formation of 9-(4-hydroxybutyl)guanine monophosphate by HSV-1 TK was measured and the rate of product formation was found to be about 10% of that found by using thymidine as a substrate. A selective inhibition of HSV-1 DNA synthesis by 9-(4-hydroxybutyl)guanine was observed in infected Vero cells. 9-(4-Hydroxybutyl)guanine had a low cellular toxicity. A weak therapeutic effect on herpes keratitis in rabbits was observed whereas cutaneous HSV-1 infection in guinea pigs and systemic HSV-2 infection in mice were not affected by this compound.

Acyclovir↗
PubMed1983

9-(3,4-dihydroxybutyl)guanine, a new inhibitor of herpesvirus multiplication.

A new compound, 9-(3,4-dihydroxybutyl)guanine, has been synthesized and its antiherpes activity determined. 9-(3,4-Dihydroxybutyl)guanine was selectively phosphorylated by herpes simplex virus thymidine kinase and had a high affinity for this enzyme, with an inhibition constant of 1.5 microM. In cell culture, replication of different strains of herpes simplex virus types 1 and 2 was inhibited to the extent of 50% by 4 to 18 microM (RS)-9-(3,4-dihydroxybutyl)guanine. The (R)-enantiomer of this compound was more inhibitory than the (S)-enantiomer. Herpesvirus DNA synthesis was selectively inhibited by (RS)-9-(3,4-dihydroxybutyl)guanine in infected cells, and a low cellular toxicity was observed. (RS)-9-(3,4-Dihydroxybutyl)guanine had a therapeutic effect when applied topically to guinea pigs with cutaneous herpes simplex type 1 infections and to rabbits with herpes keratitis. Oral treatment of a generalized herpes simplex type 2 infection in mice had a therapeutic effect.

Acyclovir↗
PubMed1982

Therapeutic effects of foscarnet sodium and acyclovir on cutaneous infections due to herpes simplex virus type 1 in guinea pigs.

The therapeutic effects of topically applied foscarnet sodium and acyclovir on cutaneous infections due to herpes simplex virus type 1 (HSV-1) were studied in guinea pigs. Foscarnet cream (3%) reduced both the cumulative vesicle score and the time for healing when HSV-1 strains C42 and 79 were tested. The application of foscarnet in cream form resulted in a dose-dependent reduction in skin virus titers and vesicle scores at concentrations ranging from 0.05% to 3%. Infections due to HSV-1 strain 79, but not those due to strain C42, were sensitive to treatment with 5% acyclovir in polyethylene glycol ointment. Topical application of 3% acyclovir in dimethyl sulfoxide on infections due to HSV-1 strain C42 resulted in a reduction in the skin virus titers, lesion scores, and the time for healing. Acyclovir, in both polyethylene glycol and dimethyl sulfoxide, was consistently less active than foscarnet cream in these animal experiments.

Acyclovir↗
PubMed1981

Antiherpes activity of [E]-5-(1-propenyl)-2'-deoxyuridine and 5-(1-propenyl)-1-beta-D-arabinofuranosyluracil.

5-(1-Propenyl)-1-beta-D-arabinofuranosyluracil has been synthesized, and this compound and [E]-5-(-propenyl)-2'-deoxyuridine have been tested for inhibition of herpes virus multiplication. Only [E]-5-(1-propenyl)-2'-deoxyuridine was found to be an active inhibitor reducing by 50% the plaque formation of herpes simplex virus type 1 (HSV-1) at about 1 muM. A comparison to the bromovinyl derivatives showed the following order of descending activity; [E]-5-(2-bromovinyl)-2'-deoxyuridine greater than 5-(2-bromovinyl)-1-beta-D-arabinofuranosyluracil greater than or equal to [E]-5-(1-propenyl)-2'-deoxyuridine greater than 5-(1-propenyl)-1-beta-arabinofuranosyluracil. HSV-1 mutants lacking thymidine kinase or resistant against acycloguanosine were resistant against [E]-5-(1-propenyl)-2'-deoxyuridine. All compounds seemed to be phosphorylated by HSV-1 thymidine kinase in a cell-free assay. The compounds were phosphorylated to a lower extent by cellular or HSV-2 thymidine kinase, and the HSV-2 strains tested were inhibited by less than 50% at 100 muM in plaque assays. A selective inhibition of HAV-1 DNA synthesis by [E]-5-(1-propenyl)-2'-deoxyuridine was observed in infected cells indicating an effect on viral DNA polymerase. [E]-5-(1-Propenyl)-2'-deoxyuridine had a low cellular toxicity and a therapeutic effect when applied topically to HSV-1-infected guinea pig skin.

Animals↗
PubMed1980

Inhibition of herpesvirus multiplication in guinea pig skin by antiviral compounds.

The effects of adenine arabinoside, cytosine arabinoside, iododeoxyuridine, ribavirin, phosphonoacetate and phosphonoformate on virus titers in cutaneous herpesvirus infections of guinea pigs have been determined and compared to their effects on lesion score. Only phosphonoacetate and phosphonoformate caused a reduction in virus titer and lesion score when the drugs were applied topically after symptoms had developed. However, unlike phosphonoacetate, phosphonoformate did not cause local skin irritation. A herpesvirus mutant, inducing a DNA polymerase resistent to phosphonoformate gave rise to an infection in which the virus titer was not reduced by phsophonoformate.

Animals↗
PubMed1980

Effect of trisodium phosphonoformate and idoxuridine on experimental herpes simplex keratitis in immunized and non-immunized rabbits.

The effect of trisodium phosphonoformate (PFA) has been compared to that of idoxuridine (IDU) when applied topically in both liquid and ointment preparations on herpetic keratitis in rabbits. Trisodium phosphonoformate had a therapeutic effect but was not as effective as idoxuridine in the vehicles tested. This was seen with both herpes-immunized and non-immunized rabbits. A herpesvirus mutant inducing a PFA restant DNA polymerase was used to infect rabbit corneas. A comparison of the effect of PFA on the keratitis caused by this resistant mutant and the wild type herpesvirus indicates that the therapeutic effect of PFA on the herpes keratitis was due to an inhibition of herpesvirus DNA polymerase.

Animals↗
PubMed1979

Effect of trisodium phosphonoformate in genital infection of female guinea pigs with herpes simplex virus type 2.

A genital herpesvirus type 2 infection in guinea pigs has been used to evaluate the inhibitory effect of phosphonoformate on the infection. An early topical treatment prevented the appearance of vesicles and histopathological changes and no virus could be recovered. When treatment, either topical or both systemic and topical, was delayed to 24 hours post infection no therapeutic effect was observed.

Animals↗
PubMed1978

Comparison of the therapeutic effects of five antiviral agents on cutaneous herpesvirus infection in guinea pigs.

Cutaneous herpesvirus infection of guinea pigs has been evaluated as a model for testing antiviral compounds. Six infected sites on each animal can be used independently for local treatment. The severity of the infection has been graded in a score system. The cumulative scores during infection and the time to healing can be used to determine antiviral effects. The effects of adenine arabinoside, cytosine arabinoside, iododeoxyuridine, ribavirin and phosphonoacetic acid on the cutaneous infection was compared. Phosphonoacetic acid was the only compound with a good therapeutic activity against herpesvirus infection, causing a reduction of both the cumulative score and the time to healing. Phosphonoacetic acid was skin irritating at 2 per cent, but at 1 per cent, which still had a good therapeutic activity, skin irritation was seen only occasionally.

Animals↗
PubMed1978

Therapeutic effect of trisodium phosphonoformate on cutaneous herpesvirus infection in guinea pigs.

When applied topically, trisodium phosphonoformate (PFA) displayed activity against established cutaneous herpesvirus infections in guinea pigs similar to that exhibited by the closely related phosphonoacetic acid (PAA); however, unlike PAA, PFA was not locally skin irritating. The therapeutic benefits of topical application of PFA were clearly evident when application was delayed for 48 h after virus inoculation, at which time lesions were well developed. The therapeutic effect was dependent on the concentration of PFA and the duration of treatment. PFA exhibited significant activity against established infections when administered intraperitoneally, although it was less effective via this systemic route than when applied topically.

Animals↗