The authors have hitherto been engaging in the study on the pattern of experimental infection and immunity of animals against the Japanese B encephalitis virus. In the study of this kind, it is most desirable to make the host-parasite system as simple as possible, and it may be best if the host of this system could be reduced to a single cell or cells.
With such an intention, many attempts were made recently and have become available, namely the attempts of virus propagation in de-embryonated chicken eggs, in monolayer cell culture of Dulbecco, in culture of suspended cells that were made free by digestion with enzymes and also those in the HeLa cell culture etc., and it has become possible to make the investigation of the host-virus relationship in a very simple host-parasite system as mentioned above.
Since Ackermann had succeeded in 1952 to propagate the influenza virus of WS strain on the Ehrlich's ascites tumor cells of mouse, it became available with good results to employ this ascites tumor as the medium of propagation for certain viruses in the study on the pattern of infection and multiplication of them.
The authors succeeded to apply as the host cell the Ehrlich's ascites tumor cell of mouse to the study on the pattern of infection with and immunity against the Japanese B encephalitis virus and could obtain some interesting results. The results obtained may be possible to be summarized as follows.
1. The Japanese B encephalitis virus (Nakayama strain) can easily propagate in the Ehrlich's ascites tumor cells of mouse that are propagating in the peritoneal cavity of mouse.
2. The Japanese B encephalitis virus seems not to exert the oncolytic effect upon the Ehrlich's mouse ascites tumor cells.
3. The propagation of the virus attains to its peak in tumor cells in the peritoneal cavity of mouse approximately 5 days after the intraperitoneal inoculation of the cells infected with the virus. Eight days after the inoculation, the titer of the virus in the ascites fluid falls remarkably and 11 days after it, the virus becomes already impossible to be recovered directly from both ascites fluid and tumor cells.
4. Eight days after the inoculation of the tumor cells infected with the virus, the neutralizing antibody against the virus which had been produced in the body of the mouse appears in the ascites fluid of it in significant titer and the virus in the ascites fluid becomes unable to get rid of the inactivating action of it.
5. If the tumor cells, in the stage when the virus had become unrecoverable at all from both the ascites fluid and the cells, were washed and made free of the ascites fluid which contains the neutralizing antibody and were inoculated anew to the mouse intraperitoneally, the virus begins to multiply again in those cells in this antibody free new medium in accordance with the propagation of the cells and appears in the ascites fluid in high titer as usual.
6. The facts above mentioned should allow us to infer that the neutralizing antibody can exert a reversible inactivating or a multiplication inhibitting effect on the virus which occupies the intracellular site in the tumor cell.
7. The mechanism, by which the neutralizing antibody acts inactivating or inhibitory against the intracellularly located virus, is not yet made clear. Above all, it remains to be elucidated, whether the neutralizing antibody can permeate into the active tumor cell or not.
8. It may be possible to be considered as follows, that in the tumor cells that are present in the medium which contains neutralizing antibody significantly, the virus can persist in the latent state for considerably long period of time. In another expression, the long persistence of the virus in the host cells after the recovery from infection may be possible to be postulated.
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