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Biomedical subjects

I Tagaya

Publications and source records attributed to I Tagaya.

At least 37 records · Page 2Linked to original sources

Aggregation of enterovirus small plaque variants and polioviruses under low ionic strength conditions.

Virion aggregation in low ionic conditions was observed with small plaque variants of Coxsackievirus type B3 and Echovirus types 4 and 11 by sedimentation and filtration methods. Inclusion of salts or DEAE-dextran into the media prevented or reversed virion aggregation. The effect of pH on aggregate formation in low ionic strength solutions was also investigated with various strains of poliovirus. Type I Sabin strain formed aggregates even at high pH, while Mahoney strains did so only below pH 6.5. Type 2 virus, Sabin and MEF1 strains, and type 3 virus, Sabin, Saukett and Suwa strains, showed an intermediate behaviour between the two type 1 strains, except MEF1-LB strain, a clone obtained from MEF1 strain under acidic overlay, which showed little tendency to aggregate. These results were compared with the degree of the d character of the strains. Besides the effect of inhibiting virion aggregation, the inclusion of DEAE-dextran into a sucrose gradient slowed the sedimentation of some of the viruses in low ionic strength solutions.

Cell Line↗

Studies on Cotia virus--an unclassified poxvirus.

This paper is a report of studies on Cotia virus; this had been first isolated in 1965 in Brazil and was subsequently shown to be a poxvirus. Cotia virus grew in a wide range of cell cultures and on the chick chorioallantois (CAM), Its growth characteristics are similar to those of other poxviruses. Microscopy showed virus factories or type B inclusions appearing before infectious progeny virus could be demonstrated. Type A inclusions appeared later, after development of progeny virus; these were shown by electron microscopy to differ from the type A inclusions of cowpox and other poxviruses and they have been termed Cotia bodies. Immunofluorescent staining also showed ring structures which appeared before the development of Cotia bodies. The growth of Cotia virus in human embryo lung (HEL) cells was sensitive to inhibitors of DNA and protein synthesis but was resistant to a concentration of rifampicin which inhibited vaccinia virus. Sharing of antigens between the Cotia virus and vaccinia virus was shown by gel precipitation tests and immunofluorescent staining. There was no cross neutralization between Cotia virus and vaccinia virus nor did anti-Cotia sera neutralize representatives of other poxvirus groups.

Brazil↗

Common antigen between coxsackievirus A 16 and enterovirus 71.

Cross immunofluorescence revealed that coxsackievirus A 16 (CA 16) shared a common antigen with enterovirus 71 (E 71). The cross reactivity of these two serotypes was also examined by complement fixation test with purified virus preparations fractionated by sucrose density gradient centrifugation and two peaks of antigenicity were detected, one being type-specific and the other cross-reacting. The common antigen was heat-stable and attributable to empty capsids. Immuno-diffusion also revealed the common antigen. Infants without antibody to E 71 developed complement fixing and precipitin antibody to E 71 after recovery from hand, foot and mouth disease caused by CA 16.

Antigens, Viral↗

Comparative studies of several vaccinia virus strains by intrathalamic inoculation into cynomolgus monkeys.

From the comparative studies of the virulence of several vaccinia virus strains by intrathalamic inoculation into cynomolgus monkeys, the following results were observed. The CV1 virus was most virulent, the New York City Board of Health, Ikeda, EM63, and Lister viruses were slightly less virulent, and DIs and LC16 viruses least virulent. The characteristic findings were widespread inflammatory lesions in the meninges and choroid plexus which were closely associated with the replication of vaccinia virus, and parenchymal lesions which might be referred to a encephalopathy in the deceased monkeys. Meningoencephalitis was, however, ofter recognized in the monkeys sacrificed at 14 days postinoculation and those dying late.

Animals↗

Factors concerning the immunity to poxvirus infection.

Two kinds of early antigens were shown in vaccinia-infected cells, one heat (56 degrees, 30 min)-stable (ES antigen) and the other heat-labile (EL antigen). Both antigens do not induce circulating neutralizing antibody in rabbits, but resistance to intradermal inoculation of active virus was observed when animals were immunized with either antigen in combination with Freund's complete adjuvant. Vaccinia-specific haemagglutinin (VHA) associated with infected cell membrane was purified and its antigenicity was also studied. Rabbits showed a good antibody response to VHA and some animals also showed neutralizing antibody, though in a small amount, to either intracellular (ICV) or extracellular (EVC) virus. Rabbits immunized with membrane antigens obtained from either VHA-positive or negative virus in combination with Freund's adjuvant showed skin restance to challenge with active virus. It was suggested that antibody against ECV might be responsible for the resistance.

Animals↗

[Smallpox].

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Humans↗

Studies on the interaction between coxsackievirus A9 and HeLa cells. I. Plaque-forming ability of coxsackievirus A9 in HeLa cell cultures.

Most of the coxsackievirus A9 (CA 9 virus) including the prototype strain formed plaques in HeLa cell monolayers under agar overlay, although they showed little or no cytopathogenicity under fluid medium. These viruses were isolated or passaged in primary cynomolgus monkey kidney (MK) cell cultures, and the infectivity of any strain in terms of plaque-forming units was much higher in MK cells than in HeLa cells, even after plaque purification of the virus in HeLa cell cultures. CA 9 virus contained in the original throat swabs as well as some clones obtained by plaque purification in MK cells failed to form plaques in HeLa cells, but virus preparations obtained after several undiluted passages through MK cells included plaque-formers in HeLa cells, suggesting that such plaque (HeLa)-forming viruses may have developed at a certain rate during multiplication of the original non-plaque (HeLa)-forming virus population in MK cells. Out of four lines of HeLa cells examined, two, including a clonal line S3, failed to support plaque formation by CA 9 virus.

Agar↗

Studies on the interaction between coxsackievirus A9 and HeLa cells. II. Mode of growth of coxsackievirus A9 in HeLa cell cultures and the effect of sulfated polysaccharide on plaque formation.

For the purpose of clarifying the mechanism of plaque formation in HeLa cell cultures by coxsackievirus A9, which does not show definite CPE in fluid cultures, we investigated the growth pattern of the virus in HeLa cells, comparing plaque (HeLA)-forming and non-plaque (HeLa)-forming viruses. It was revealed that the yield of both viruses per cell was nearly the same, but non- plaque (HeLa)-forming virus was far less efficient in infecting HeLa cells. Dextran sulfate was effective in releasing more virus from cells, when HeLa cell cultures were infected with plaque (HeLa)-forming virus, but not in cultures infected with non-plaque (HeLa)-forming virus. From these experimental results, the mechanism by which plaques are formed in HeLa cell cultures by coxsackievirus A9 was discussed.

Adsorption↗

Picornaviridae.

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Enterovirus↗