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.

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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.

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Attempts were made to isolate virus from throat swabs obtained from outpatients suffering from acute undifferenciated febrile illnesses who visited a pediatric clinic in Fujinomiya City, Shizuoka Prefecture.
Specimens were collected over 6 year period, from March 1968 to March 1974, for virological and epidemiological examinations ; and the following conclusions were drawn.
1. Eight hundred and eighty two strains of various viruses were isolated from 4, 972 specimens. The species and type of isolated virus were consisted of influenza A (H3N2) and B; parainfluenza virus type 1, 2 and 3; adenovirus type 1, 2, 3, 5 and 6; enterovirus type, Cox.A7, 9 and 16; Cox.B1, 2, 3, 4, 5 and 6; Echo type 9, 11 and 17; poliovirus type 1 and 2; and herpes simplex virus.
2. Virological and serological investigations on patients of respiratory disease in summer of revealed that influenza B virus continued to be prevailing during summer 1973, suggesting the continuance of transmission of influenza virus in the period when influenza virus is not usually prevalent.
3. Parainfluenza virus was found to have a seasonal predilections, depending on its type. It is of interest that such closely related viruses have different seasonal variations of prevalence.
4. Each clinical type of disease occurred during various seasons. The common cold, bronchitis, catarrhal croup, exanthema subitum, tonsillitis, asthmatic bronchitis, and pneumonia were observed throughout the year. Tentative diagnosis of acute febrile illness, tentative diagnosis of acute exanthematous disease, pharyngo-conjunctival fever, hand foot and mouth disease, herpangina, and aseptic meningitis occurred mainly in the summer. Influenza were mainly seen in the winter.
5. There was no doss relationship between clinical types of disease and viruses isolated. Both virus recovery and the clinical type of disease were related to the seasonal fluctuations.
6. A cyclic infection and the interference phenomenon induced by enterovirus were discussed virologically and epidemiologically.
7. Epidemiological studies were perfromed on Cox.B6 isolated from patients with disease of the respiratory tract, and on poliovirus derived from the live vaccine.

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