From the end of the year 1947 to the early summer of 1948, a diarrheal disease of infectious nature prevailed in Japan. The disease appeared fairly abruptly and when it was recognized as a serious public health problem, it had already been spread almost all over Japan. It stimulated research workers as well as public health officers as a hitherto unknown disease entity. Human volunteer experiments conducted by some Japanese workers (Kojima et al., 1948; Yamamoto et al., 1948) revealed that the etiological agent of the disease was filtrable. The disease was called infectious diarrhea by Kojima et al. (1948) .
It was reported by Gordon, Ingraham and Korns (1947) that a diarrheal disease whose clinical features seemed to be almost the same as those of the disease in Japan, draw attention frequently in the form of institutional outbreaks, but sometimes attacked families in localized areas mostly in 1946 and 1947 (see also Ingalls and Britten, 1951; Britten, Rubenstein, Raskin and Strassmann, 1951; Smillie, Howitt and Denison, 1948) . The disease was at first named epidemic gastroenteritis by Gordon, Ingraham and Korns, but later afebrile infectious nonbacterial gastroenteritis in order to distinguish from the other form of diarrheal disorder, namely febrile infectious nonbacterial gastroenteritis (Gordon, 1954; Jordan, Gordon and Dorrance, 1953; Gordon, Meneely, Currie and Chicoine, 1953) .
The afebrile infectious nonbacterial gastroenteritis seems to be still continuing to occur from time to time in several places in the United States, according to Gordon (1954) and Gordon, Ingraham, Korns and Trussell (1949) . The situation appears to be the same for the infectious diarrhea in Japan, because it is reported that several localized occurrences of this disease were found each year thereafter (Fukumi, Ishimaru and Yamaguchi, 1948; Ishimaru, 1950; Kojima, Fukumi and Ishimaru, 1953), some of which were identified as such by human volunteer experiments (Fukumi, 1955; Hirayama, Fukumi, Nakaya, Kusano, Aoyama, Kagawa, Noguchi and Murate, 1955; Ishimaru, Koike, Amamiya, Hagihara, Fukumi and Nakaya, 1955) .
There is no positive evidence of the existence of this disease in Japan before or during the Second World War, and from several epidemiological points of view, it may be reasonable to consider that the infectious diarrhea in Japan and the of ebrile infectious nonbacterial gastroenteritis in the United States are an identical disease and that its occurrence in Japan had some connections with the epidemics in the United States.
In order to take the hypothesis just mentioned into consideration, it is, however, necessary to compare both the diseases not only from clinical but also from etiological viewpoint for identification.
In our previous report (Kojima et al., 1948), it was established that patients recovering from infectious diarrhea became immune to refeeding of infected feces at least 1-3 months after recovery, though neutralizing antibodies were not evidenced by our experimental procedure. Therefore, it is considered to be possible to compare both the diseases by cross infection experiments.
In the year 1954 we received a virus strain of afebrile infectious nonbacterial gastroenteritis, Marcy strain, from Dr. Irving Gordon (Division of Laboratories and Research, N. Y. State Department of Health, Albany at that time), who asked one of us (H.F.) to perform studies for comparison of both the diseases. The present paper is devoted to the description of our experimental results using human volunteers in order to solve the problem just mentioned above.

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Adams (1954) defined abortive infection as the loss of the plaque forming potential of infected bacteria under conditions which do not result in destruction of either free phage or uninfected bacteria. His discussion was primarily concerned with the abortion of infection caused by certain chemical agents, for instance, as 5-methyl tryptophane, but the purpose of his paper was, as he stated there, to look for generalization, if any, to be drawn concerning this phenomenon. Benzer (1952) discovered a type of abortive infection which proceeded in starved bacterial cells infected with bacteriophage T2r, and a more extensive study of this kind of phenomenon was conducted by Gross (1954a; 1954b) . At first, the term “abortive adsorption” was used by Benzer for the phenomenon, but Gross proposed to call it “abortive infection” because of the lack of experiments permitting the isolation of the specific phase of infection during which the loss of infective centers occurred.
The phenomenon called abortive infection by Gross is actually concerned with the incapability of a fraction of the starved bacterial population ofEsherichia. coil, K12 to support the synthesis of bacteriophage T2r. However, Lwoff (1953) employed the term“abortive phage development”in his review of lysogeny, where a strain of B. megateriumlysogenized by a bacteriophage is subjected to lysis with production of no bacteriophages when induced by ultraviolet irradiation. So far unknown is a relation between two phenomena both called“abortive”.
The invasion of the bacteriophage into a host cell is another problem. Hershey revealed that the phage DNA is introduced into a host cell through the tail of the phage, with which this is attached to its host cell (Hershey, 1953) . Puck (1954), Puck, Garen and Cline (1951), and Puck and Sagik (1953) analyzed experimentally several factors involved in cell attachment and penetration by bacterial viruses; primary virus cell attachment, which occurs through electrostatic binding, is followed by virus penetration, of which the first step is thought to be principally constituted by a phenomenon of splitting the virus into protein and DNA particles. According to them completion of virus penetration is influenced upon by several factors. In a normal process the splitting of the virus into protein and DNA parts is immediately followed by the injection of the splitted DNA into the cell, but in some abnormal cases the splitted DNA may be liberated into the external medium.
Luria and Steiner (1954) investigated the role of calcium ion in the first step of bacteriophage T5 infection. Phage T5 adsorbed on its host cell is inactivated fairly rapidly in the absence of calcium or magnesium ion and even in the presence of adequate concentrations of calcium the penetration process is rather slow requiring several minutes for its completion. This result agrees quite well with Lanni's finding (Lanni, 1954) obtained by a different procedure.
During the experiments concerning host-range mutation of T2 bacteriophage, a mutant ofE. coli, strain B was obtained whose behavior towards T2 phage was fairly peculiar and may throw some light on the phenomenon of abortive infection as well as penetration process of T2 bacteriophage. The present paper is devoted to describe the analyses of the process of abortive infection of T2 phage in the mutant of E. coli, strain B.

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Except for a few cases of successful cultivation in chemically defined media of special types of cells as recently reported by Healy et al. (1955) and Evans et al. (1956), it is generally the case that separated animal cells can not be grown in vitro without such materials of living origin as embryo extract or serum. The effect of embryo extract on growth of chick embryonic fibroblasts in tissue culture was first noticed by Carrel (1913) . Fischer et al. (1943) analyzed embryo extract by dialyzation and later referred to the effective nondialyzable fraction as embryonin, supposing the essential substance to be nucleoprotein (Fischer et al., 1948) . This supposition was validated by later investigations carried out by Davidson et al. (1945), Hoffman et al. (1951), Kutsky (1953), Katsuta et al. (1954) and many others, the growth-essential substance being proved to be nucleoprotein. These works chiefly pursued the efficacy of embryo extract on chick embryonic fibroblasts. On the other hand, however, Sanf ord et al. (1952) tested ultrafiltration-treated fractions both of chick embryo extract and of horse serum on the mouse L strain cells and demonstrated that the protein-containing fraction of chick embryo extract could be eliminated from culture fluid without losing the growth-promoting effects. It is thus considered that the manner in which embryo extract works for cell growth in vitro is variable according to the cell type.
In the present experiments was studied the role of chick embryo extract on the HeLa strain cells originated from a human epidermoid carcinoma of the cervix, on the basis of estimation of cell population, and it was found that the embryo extract was not essential for the cell proliferation but exerted a certain effect on the growth mode of cells.

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The idea that the two phenomena, host-range mutation and host-controlled variation may be merely superficially different from each other, but principally two sides of a single matter, arose to us at first when we were studying “semi-resistance” of the bacterium to the bacteriophage (Nojima and Fukumi, 1954b) . It was further developed when the so-called host-range mutations of T3 bacteriophage were investigated from this point of view (Fukumi and Nojima, 1954) . The fundamental difference of our thought from the current view of host-range mutation lies in the following point; namely, if the bacteriophage a possesses the inf ective titers of 10⁹/cc on the host microorganism A and of 10³/cc on the resistant host A/a, one usually understands according to the current view that 10³ particles of the host-range mutant of phage a being capable of attacking the resistant host A/a exists among 10⁹ particles of the original phage a, while according to our view, it is explained so that the phage a possesses 10^-6 of efficiency of plating (EOP) on the resistant host A/a in comparison with its value 1 of EOP on the original host A.
The fact that a number of phenomena concerning host-range mutation of T3 phage can be explained only partially by the current theory has already reported by Fraser and Dulbecco (1953) and Hershey, Garen, Fraser and Hudis (1954) besides us. However, no reasonable explanation has been presented so far by any of the workers.
The presentation alone of the facts that are impossible to explain is not of constructive nature, and as even the consideration described by us in the previous paper (Fukumi and Nojima, 1954) does not include, fundamentally speaking, any understandable analysis from genetical point of view, it may have at most confused or irritated some workers.
In the present paper, we are going to present aa theory capable of explaining genetically the difficulties mentioned above. The theory has been constructed by us from the suggestions of Hershey, Garen, Fraser and Hudis (1954), and of Demerec (1956) . The former workers have suggested that the host-range mutants of T3 bacteriophage arise by interactions between phage and bacterium, possibly in the nature of genetic substitutions, while the latter have explained the transduction by the cross-over between the host genes and the phage genes.
Before the theory is presented, some data concerned with the host-range mutations of T1 phage, which are also impossible to explain by the current view will be described at first.

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During the summer of 1955 an outbreak of the Far Eastern urticating moth, Euproctis flava Bremer, occurred in an extensive area of Japan. The urticating spicule, s of both the caterpillars and the moths cause itching for human skin, and frequently produce rashes and swellings even accompanied with fever.
During the course of our investigation the caterpillars were found to be attacked by polyhedrosis, of which the polyhedra were formed in the nuclei. At the same time small outbreaks of the tea-tussock moth, Euproctis pseudocons persa Strand have occurred, and, allied polyhedral disease of the larval insects was also recognized. This paper deals with the pathology and the viruses of the polyhedroses of these Lepidoptera.

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