1961 Volume 14 Issue 3 Pages 109-120
Since the year of 1950 or probably a little earlier, a kind of hemagglutinating virus has been prevalling in laboratory mice in Japan and often disturbed laboratory works for viral experiments, especially those dealing with virus isolation using mice (Fukumi et al., 1954) . The shape and size of this virus were studied in detail by the present authors and on that occasion the virus was named as hemagglutinating virus of mice (HVM) (Nishikawa and Fukumi, 1954) . Sasahara et al. (1954) found that the virus was also the cause of a natural disease of pigs with febrile response in Japan. Thus, it was known that the virus was widely distributed in Japan either in laboratory or domestic animals, and consequently various names were employed for it by many workers, which caused some confusion especially in the literature. Accordingly, the Japanese Society of Virologists established a committee for nomenclature of this virus and thus “hemagglutinating virus of Japan (HVJ) ” was proposed as the name of the virus. This virus seems to be widely called Sendai virus outside of Japan since Jensen et al.'s publication (1956) though they proposed the name of influenza D virus.
The same virus was reported to be isolated from human newborn pneumonitis by Kuroya et al. (1953) . This report was considerably widely acquainted with and seems to have played an important role in letting one believe that this virus be pathogenic to human beings. But, as we already pointed out in a previous publication (Fukumi et al., 1959), they used laboratory mice for virus isolation and at that time the virus was reported to be isolated frequently from laboratory mice in many areas of Japan and, as far as we were told, they did not succeed in isolating this virus after they changed their methods from mice to embryonated eggs. These situations may led one suspect that the virus isolated by them was derived from the mice employed by them, and not from the human patients. Hence, it seems to be very dangerous to conclude from their report that this virus is responsible for some disorders of human respiratory tracts.
Since Kuroya et al.'s report, however, several papers were published which attributed a certain symptoms of upper respiratory tract to Sendai virus (Fujii et al., 1955; Yanari, 1958) . But their conclusion was mostly drawn from serological findings by evidencing antibody rise against Sendai virus at convalescence, and as Sendai virus shares antigen in common with HA2 virus which was certainly evidenced to be pathogenic to human beings, as has recently been shown (Chanock et al., 1958; Fukumi et al., 1959), it is very difficult to draw such a conclusion merely on a serological basis. Further difficulties have been presented by the findings of DeMeio et al. (1957, 1958), that the antibody rise against Sendai virus is observed in mumps virus infections or some other diseases such as infectious mononucleosis. Thus, according to our opinion, it is not conclusive for Sendai virus to cause natural infections in human beings, while it is quite certain that the virus is sometimes responsible for diseases in swine and laboratory animals. During our observations in laboratory mice which lasted for about 2 years, we recognized twice epidemics of Sendai virus infection among them (unpublished data), being confirmed by virus isolation experiments and serological investigations.
Andrewes et al. (1959) have proposed a nomenclature in which parainfluenza virus 1 is applied to include both HA2 and Sendai virus together. If this nomenclature should be accepted, these two viruses must not be confounded with each other, because not only their antigenic, but also biologic characteristics are definitely different from each other besides the difference of their ecological and pathogenic behaviors in the natural world as has been cited above in detail.