Simian virus 40 (SV40) has been well known to give rise to specific vacuoles in the cytoplasm of cultured kidney cells from special kinds of monkey, such as African green monkey (Sweet & Hilleman, 1960), patas and baboon monkeys (Hsiung & Gaylord, 1961) . The remarkable accumulation of small vacuoles in the cytoplasm of infected cells is so characteristic that SV40 was given another name, the “ vacuolating virus ”. It has been recognized that kidney cell cultures of rhesus monkeys show neither vacuolation of the cytoplasm nor any other signs of cytopathic effect (CPE), although characteristic nuclear changes were revealed by hematoxylin-eosin staining and a good yield of infectious particles was usually obtained in these cultures. No reliable observations on the growth of SV40 in cynomolgus monkey kidney cell cultures have ever been reported. During the course of the studies on SV40 in our laboratory, it was found that some batches of cynomolgus monkey kidney cell cultures manifested characteristic vacuolation of the cytoplasm after infection with SV40, while other batches were apparently unaffected. This communication deals with the mode of growth of SV40 in cynomolgus monkey kidney cells with evidence which determines the vacuolation in the cytoplasm as specific CPE caused by SV40.
Effort has been made to purify Japanese encephalitis (JE) virus from suckling mouse brains infected with the Nakayama strain. The brain contains so many extractable contaminating materials that purification of the virus from brain suspension by mere repetition of fractional centrifugation has been difficult (Kitaoka, 1955) . Recently, Nojima et al. (1964) reported a purification procedure of JE virus from infected suckling mouse brains by adsorption technique on hydroxyapatite column. The recent progress of sedimentation techniques has opend a simple and efficient way for purification of many animal viruses from infected tissues and tissue culture cells. The present paper will describe in detail the purification procedure of JE virus from infected suckling mouse brains by the protamine treatment, fractional centrifugation and sucrose gradient centrifugation. Also the structure of virus particles will be discussed in regard to hemagglutinating (HA) and complement fixing (CF) substances and infectious principle.
In the preceding paper (Takasaka et al., 1964) which dealt with the epidemiology of natural infection of Shigella bacilli in cynomolgus monkeys, the authors have stated that Shigella bacilli may have some causative role in the development of dysentery in monkeys. If this disease can be reproduced in monkeys experimentally with success by means of oral administration of the bacilli, it will aid probably in clarifying the etiology, pathogenesis, treatment and prevention of dysentery in monkeys. Moreover, it will be available as an experimental model to elucidate a number of unsolved problems relating to human bacillary dysentery, because the production of dysentery of essentially the same type as human bacillary dysentery is impossible in ordinary laboratory animals — such as rabbits, rats, mice, guinea pigs and dogs, etc. — by any known method of infection, and spontaneous dysentery in monkeys closely resembles human bacillary dysentery in its feature. Although many works concerning the experimental infection in monkeys with Shigella bacilli have been reported by Soviet investigators (Tumanian, 1956), they have not described in full detail the methods and procedures of experiments including the conditions of monkeys used as well as the results obtained. Therefore, the present authors are unable to evaluate properly their investigations. Dack (1934) reported that a freshly isolated virulent strain of Shigella organisms produced an infection in an isolated loops of the colon of rhesus monkeys resulting in a profuse bloody mucous discharge. However, these monkeys showed no signs of infection in the bowel except in the isolated segments of colon. Also Branham et al. (1949) were unable to establish clear-cut infection with Shigella dysenteriae in mulatta macaques. In Japan, Ebira (1937) reported a study of Shigella infection using monkeys, but his study may not be strictly criticized or appreciated since it was done when the knowledge of the monkey itself used as an experimental animal had not been so sufficient in Japan. Recently, Hayashi and Iwahara (1962, 1964a, b, c) published papers in which they concluded all monkeys used had developed clinical symptoms and pathological changes of dysentery. Their findings, however, evidently differ from those of spontaneous dysentery in monkeys which the present authors usually observe at NIH; the former showed severe systemic reactions while the latter had not such reactions but limited changes in the large intestine. In the present study, the authors tried to produce dysentery in cynomolgus monkeys under certain experimental conditions that were controlled as sufficiently as possible on the basis of the present knowledge of monkeys used for medical and biological purposes. Pathological findings of this work will be published in the subsequent paper (Ogawa et al., 1964) .
Since 1960, a diarrheal disease, presumably related to Shigilla infection, has been observed among cynomolgus monkeys (Macaca irus) during quarantine at the Division of Animal Care, Branch Laboratory in Murayama, the National Institute of Health. Muto et al. (1963) and Takasaka et al. (1964) reported results of an epidemiological survey of the disease which placed emphasis upon the carrier status of Shigella bacilli. Honjo et al. (1964), furthermore, have succeeded in experimental infection of healthy monkeys with Shigella flexneri 2a isolated from the diarrheal animals. The present work offers the histopathological observation made on the natural and experimental Shigella infections of monkeys, with additional survey on human materials of Shigellosis diagnosed clinically as Ekiri. The latter was made for the purpose of comparison of Shigellosis between monkeys and human beings.