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Your search keyword '"Kinase activity"' showing total 2 results
2 results on '"Kinase activity"'

1. Pathogenicity of Acyclovir-Resistant Herpes Simplex Virus Type 1 from an Immunodeficient Child

Author

Paul M. Keller, M. H. St. Clair, Wilfert Cm, David Walter Barry, C. McLaren, Laura T. Gutman, and C. D. Sibrack

Subjects
Male, Simplexvirus, Thymidine kinase activity, food.ingredient, Adenosine Deaminase, viruses, Microgram, Acyclovir, Mice, Nude, Virulence, Biology, medicine.disease_cause, Mice, food, medicine, Animals, Humans, Immunology and Allergy, Mice, Hairless, Mice, Inbred BALB C, Severe combined immunodeficiency, Idoxuridine, Immunologic Deficiency Syndromes, Infant, Drug Resistance, Microbial, Herpes Simplex, medicine.disease, Virology, Infectious Diseases, Herpes simplex virus, Thymidine kinase, Female, medicine.drug
Abstract

Sequential isolates of herpes simplex virus type 1 (HSV-1) from a child with severe combined immunodeficiency were examined for sensitivity to acyclovir. Early intravenous courses of acyclovir resulted in dramatic clinical improvement and were associated with the isolation of sensitive strains of HSV-1 (ID50[dose inhibiting 50% of control plaques], 0.010-0.106 microgram/ml), whereas later recurrences following intravenous, oral, and ophthalmic therapy were characterized by low-grade chronic lesions (ID50, 1.04-9.43 microgram/ml) that were unresponsive to acyclovir despite serum levels of up to 10.45 microgram/ml. Diminished sensitivity was associated with reduced viral thymidine kinase activity, and linked resistance with idoxuridine was detected in the isolates from the patient's eye. Intracerebral and cutaneous snout inoculation of a resistant isolate into BALB/c, hairless, and athymic nude mice revealed a 100- to 1,000-fold decrease in virulence as compared with an early sensitive isolate. Acyclovir-resistant HSV-1 can emerge in certain clinical settings but may be associated with diminished virulence.

Published
1982

2. Role of metabolism in pathogenesis of bacteremia due to Diplococcus pneumoniae in rabbits.

Author

Guckian, James C. and Guckian, J C

Subjects
AMINO acid metabolism, HEART metabolism, ADENOSINE triphosphate metabolism, PROTEIN metabolism, GLUCOSE metabolism, ACETIC acid, ADENOSINE diphosphate, ANIMALS, BIOLOGICAL models, CARBOHYDRATE metabolism, CARBOXYLIC acids, GENETIC disorders, GLYCOGEN, ISOTOPES, LACTATES, LIPID metabolism disorders, LIVER, LUNGS, MUSCLES, RABBITS, SEPSIS, STREPTOCOCCAL diseases, STREPTOCOCCUS, PENICILLIN G
Abstract

Since the lethal factors in most bacterial infections have not been defined, the role of metabolic alterations was investigated. Bacteremia was produced in rabbits by infection with Diplococcus pneumoniae, and the animals were grouped by severity of the disease as determined by progressive increments in the level of bacteremia, concentration of lactate in whole blood, and change in body temperature. Adenosine triphosphate and adenosine diphosphate in blood, liver, heart, and skeletal muscle were normal. Hepatic glycogen was variably decreased, and 45% of the animals were hypoglycemic despite normal hepatic glucogenesis. Concentrations of lactate in heart and liver increased. In-vitro oxidation of glucose, acetate, and pyruvate decreased in liver only. Glycolysis was normal in liver, heart, and muscle, but it was markedly increased in the lung. Hepatic synthesis of the triglyceride from acetate increased markedly. Hepatic microsomal protein synthesis apparently was normal, but amino acids in plasma, liver and skeletal muscle were increased. Complex multifaceted alterations in metabolism occurred. It is doubtful that anyone of these could be responsible for death, but the role played by these changes as a whole is unknown. [ABSTRACT FROM PUBLISHER]

Published
1973

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