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Biomedical subjects

K F Soike

Publications and source records attributed to K F Soike.

71 records · Page 4Linked to original sources
PubMed1982

Acyclovir in the treatment of simian varicella virus infection of the African green monkey.

Acyclovir (9-(2-hydroxyethoxymethyl)guanine) administered as an intramuscular formulation twice daily at a dosage of 100 mg/kg per day prevented the development of disease in African green monkeys inoculated with simian varicella virus. Viremia, appearance of a vesicular rash, and elevations of serum transaminases, each indicative of infection, were suppressed by acyclovir treatment. Plasma concentrations of acyclovir were measured and showed rising levels after repeated intramuscular injection with a prolonged period of absorption of acyclovir into the plasma circulation. Investigation of antiviral efficacy after either intramuscular or intravenous acyclovir treatment showed both routes of administration to be effective in inhibiting simian varicella virus infection at the 100 mg/kg per day level. However, intravenous acyclovir 50 mg/kg twice daily did result in elevated values of blood urea nitrogen, creatinine, and serum transaminases.

Acyclovir↗
PubMed1982

Coxsackievirus B4 nephritis in the squirrel monkey.

Seventeen squirrel monkeys (Saimiri sciureus) were experimentally infected with Coxsackievirus B4, and the kidneys, as well as other organs, were studied for pathological changes induced by the virus. Seven (41%) of these monkeys developed renal lesions--interstitial and glomerular. The Coxsackievirus was identified in 4 of these 7 monkeys (by isolation from the renal tissue in 2, by immunofluorescence staining of viral antigen in 1, and by electron microscopic finding of viral particles in 1). The renal lesions produced by Coxsackieviral infection described in this report resemble those seen in renal disease in man. These findings support the concept that viruses can produce glomerular and interstitial renal disease. This report also describes a good animal model for the study of viral disease of the kidney.

Animals↗
PubMed1981

Acyclovir treatment of experimental simian varicella infection of monkeys.

Replication of simian varicella virus (SVV) in Vero cell cultures was inhibited by acyclovir, 9-(2-hydroxyethoxymethyl)guanine (ACV), at a concentration of 10 micrograms/ml in culture medium. Intravenous administration of ACV at 10 mg/kg twice a day for 10 days or 15 mg/kg three times a day for 5 days to patas monkeys (Erythrocebus patas) beginning 48 h after SVV inoculation blocked the appearance of rash and other clinical symptoms but did not affect viremia. ACV treatment of African green monkeys (Cercopithecus aethiops) at 10 mg/kg twice a day by intravenous injection beginning 24 or 72 h after SVV inoculation and continuing for 10 days had no effect on clinical symptoms, including the development of rash, or on the appearance of viremia. The minimal therapeutic results could be due to the observation that doses of 10 or 15 mg/kg produced plasma levels of ACV which were lower than 5 micrograms/ml, the concentration that inhibited SVV multiplication in vitro, and decayed rapidly.

Acyclovir↗
PubMed1980

Ineffectiveness of adenine arabinoside and adenine arabinoside 5'-monophosphate in simian varicella infection.

Adenine arabinoside and adenine arabinoside 5'-monophosphate (ara-AMP) have been evaluated for antiviral activity against simian varicella virus infection in monkeys. In a preliminary study for toxicity, intramuscular injection of ara-AMP at 15 mg/kg per day as a single injection for 5 days to two normal patas monkeys caused no detectable local reaction, no weight loss or changes in serum transaminase levels, and no hematological abnormalities. When this dose was given in the treatment of four simian varicella virus-infected patas monkeys, no effect was observed on the clinical course of infection, as compared with four infected monkeys which received phosphate-buffered saline. Treatment was begun 43 h after virus inoculation and was continued for 16 days. Toxicity of intravenously administered ara-AMP at 100 to 50 mg/kg per day for 5 days to pairs of uninfected patas monkeys was evident by hematological and hepatic histological alterations, as well as the death of one monkey in each pair. No gross evidence of toxicity occurred in two monkeys which received 20 mg of ara-AMP per kg per day. The antiviral efficacy of intravenous treatment was studied in groups of four African green monkeys which received adenine arabinoside at 15 mg/kg per day or ara-AMP at 18.4 mg/kg per day. Drug administration began 48 h after inoculation with simian varicella virus and continued for 10 days. The monkeys that received treatment did not respond to infection differently from four infected control monkeys similarly treated with phosphate-buffered saline.

Animals↗
PubMed1980

Susceptibility of nonhuman primate species to infection by simian rotavirus SA-11.

Enzyme-linked immunosorbent assay examination of sera from three nonhuman primate species demonstrated the presence of antibody reacting with simian rotavirus SA-11 and calf rotavirus C486. The occurrence of this antibody in sera from adult, wild-caught animals suggests natural rotovirus infection. The occurrence of antibody was highest in the chimpanzee and declined, respectively, in the rhesus macaque and in the squirrel monkey. Inoculation of three infant rhesus macaques, a nursery-reared chimpanzee, and a cesarian-derived nursery-reared baboon with SA-11 virus resulted in enteric infection, with virus excretion beginning 48 to 72 hours after oral administration of the virus. Clinical disease, as manifested by diarrhea, was observed only in the chimpanzee. Inoculation of ten squirrel monkeys, from 30 to 191 days old, induced infection only in the monkey inoculated at 30 days of age. This monkey became ill within 48 hours after viral administration and was euthanatized. Necropsy demonstrated a generalized infection, with virus recovered from lung, liver, kidney, spleen, and intestine. The remaining nine inoculated squirrel monkeys failed to develop enteric infection and did not respond with antibody to SA-11 virus.

Animals↗
PubMed1978

Phosphonoacetic acid in the treatment of simian varicella.

Phosphonoacetic acid inhibited replication of simian varicella virus (Delta herpesvirus) in tissue culture. The drug was tested in patas monkeys 40 h after infection with Delta herpesvirus. A total of 200 mg/kg per day was given intramuscularly, divided into two doses every day for a total of 10 days. The treated monkeys were protected from clinical illness, and Delta herpesvirus was not recovered from their lymphocytes. Complement-fixing and neutralizing antibody titers were significantly lower in phosphonoacetic acid-treated monkeys than in the untreated controls. In animals given the drug alone, there was dermatitis and blackening of the skin and hair, serum glutamic oxalacetic transaminase and serum glutamic pyruvic transaminase enzymes were significantly increased, and liver biopsy revealed diffuse cytoplasmic swelling and granulation of the hepatocytes. The therapeutic range of this drug should be studied carefully before considering its use in severe varicella-zoster infection in humans.

Animals↗
PubMed1977

Effect of interferon respiratory infections of animals.

Several animal models are available for the evaluation of interferon in respiratory virus infections. Considerable variability exists among the respiratory viruses with respect to sensitivity to exogenous interferon or induced endogenous interferon. Due to this apparent variability, combinations of interferon with immune serum and chemotherapeutic agents may provide a means of more efficient control of respiratory infections.

Animals↗
PubMed1976

Infection of newborn and fetal hamsters induced by inoculation of LuIII parvovirus.

The LuIII parvovirus was adapted to the newborn hamster and produced a systemic infection with massive intestinal hemorrhage. Inoculation of pregnant hamsters lead to transplacental infection of the fetuses and abortion. Most fetal deaths were observed in animals inoculated on days 8 and 10 of gestation. Virus was recovered from dead fetuses, placentas, and viable fetuses. Histological lesions were found in the heart, liver, kidney and CNS of infected fetuses.

Animals↗