Biomedical subjects
Publications and source records attributed to J W HARTLEY.
A virus having the characteristics of the papovaviruses was isolated from several naturally occurring cottontail papillomata. Serologic and animal inoculation studies indicate that it is not Shope papilloma virus, but a previously undescribed, nonpathogenic agent of cottontail rabbits.
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The relationship of polyoma (parotid tumor) virus infection to spontaneous and x-ray induced lymphocytic neoplasms (leukemia) in mice has been studied in two sublines of the high leukemic AKR strain, in the high leukemic C58 strain and in the x-ray responsive C3Hf/Bi strain. There was found to be no correlation of hemagglutination-inhibiting (HI) antibody with leukemia appearing at various times throughout life, and there was no evidence of increased risk of developing leukemia in mice with prior antibody to polyoma virus. Virus isolation experiments accomplished with AKR leukemic mice showed that HI antibody status of these mice had the same significance with regard to presence or absence of detectable virus as was previously observed for non-leukemic mice from infected colonies. The results of this study were interpreted as supporting the concept that the repeated association of polyoma virus and experimental transmission of leukemia is fortuitous.
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Treatment of guinea pig erythrocytes with types A and B influenza viruses rendered them inagglutinable by polyoma virus; also, the inhibitory effect of ovomucin on polyoma virus hemagglutination was destroyed by pretreatment of the ovomucin with various myxoviruses. These results indicate that polyoma virus and myxovirus erythrocyte receptor sites are identical. However, no destruction by polyoma virus of its own or of myxovirus receptors or inhibitors was detected. No serologic relationship was detected between polyoma virus and members of the myxovirus group; differences in size and stability further indicate their distinctness. No evidence was found of biologic or serologic relationship of polyoma virus with encephalomyocarditis virus or mouse encephalomyelitis virus.
Mouse polyoma virus was stored at 4 degrees and -60 degrees C. for 8 weeks without any loss in hemagglutination or infectivity titer; storage at 37 degrees for 8 weeks reduced infectivity titer by approximately 2.5 log(10) units. Repeated freezing and thawing of infectious tissue culture fluid had no effect on virus titer. The stability of the virus to storage for 1 week at 4 degrees C. was unaffected by suspension of infected tissue culture fluid in saline, demineralized distilled water, or 5 per cent horse serum in Eagle's basal medium. Heating the virus for 30 minutes at 60 degrees C. had no effect on infectivity and hemagglutination titers. Heating at 65 degrees C. for 30 minutes produced a 3 log unit loss of infectivity and a 4-fold decline in HA titer, and heating at 70 degrees C. for 30 minutes usually produced complete inactivation of infectivity and HA. The virus was resistant to ultraviolet irradiation; ultraviolet irradiation for 2 hours caused a 4 log unit decrease in infectivity titer without affecting the HA titer. The virus was resistant to exposure to 2 per cent phenol and 50 per cent ethyl alcohol but was inactivated by 100 per cent ethyl alcohol, and ethyl alcohol-iodine mixtures. Lyophilization had no effect on the stability of the virus.
Eight mouse colonies were surveyed for prevalence of antibody to mouse polyoma virus. Frequency of HI antibody varied from 0 to 84 per cent in adult mice in different colonies. Antibody was infrequent in mice less than 3 months of age, and increased in frequency with age. There was no evidence that infection was specific for particular mouse strains. The highest frequency of infection was found in colonies in which breeding mice are housed in proximity to mice inoculated with polyoma virus or passage tumors, and within an infected colony, the incidence of infection was greatest in rooms housing mice inoculated with polyoma virus. Mice from a colony free of antibody became infected when held in room or cage contact with virus-inoculated mice, but at very low rates except in mothers of inoculated litters. These results were interpreted as indicating that artificial contamination of the environment is an important factor in determining the prevalence of infection in the colonies observed. There was no correlation between polyoma infection and spontaneous leukemia in AK. mice.
THREE PROCEDURES HAVE BEEN COMPARED FOR USEFULNESS IN TITRATION AND DETECTION OF POLYOMA VIRUS: production of cytopathic effect (CPE) in mouse embryo tissue culture, production of HI antibody after inoculation into weanling mice (MAP test), and production of tumors in suckling hamsters during a 3 to 5 week observation period. The tissue culture and mouse antibody production tests were generally comparable in sensitivity, reproducibility, and time required to obtain results. Titration by tumor production in suckling hamsters was not suitable for quantitation because of marked variation in susceptibility among animals. Virus was detected in tissues of normal mice from spontaneously infected colonies by either production of CPE in mouse embryo tissue culture or by the MAP test; virus was found in organs of 15 (58 per cent) of 26 mice with antibody, and 2 (8 per cent) of 24 mice without antibody.