Salmonella phage ε¹⁵ goes under host-controlled variation (Uetake and Nakagawa, 1960; Toyama and Uetake, 1961; Uetake et al., 1962). ε¹⁵ propagated on Salmonella anatum (=A) shows EOP (efficiency of plating) of about 10^-2 on cells of Salmonella butantum (=I-1), while ε¹⁵ propagated on cells I-1 shows EOP of 10^-4 on cells A.
However, when growing cells of I-1 are heated at 49°C for 2-3 minutes, transferred back to 37°C, and infected with phage ε¹⁵[A], the proportion of plaque formers to infected cells increases up to 4-6×10^-1. It indicates that thermolabile factor (s) is responsible for HCV.
When cells of I-1 are heated after infection with ε¹⁵[A], the heat effect on EOP decreases with increasing time elapse prior to heating, indicating the irreversible inactivation of injected phage DNA.
When cells I-1 are heated at 49°C for 3 minutes, transferred back to 37°C, and thereafter aliquots are infected with ε¹⁵[A] at time intervals, elavated EOP falls down back to original 10^-2 in about 30 minutes, suggesting de nove synthesis of the responsible factor (s). This recovery from the heat effect is completely suppressed by blocking protein synthesis with chloramphenicol, while not affected by clocking DNA synthesis with mitomycin C.
These findings altogether indicate that some thermolabile factor (s) of protein nature is responsible for HCV, which may possibly inactivate injected DNA of restricted phage.

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The present paper describes the infectivity of RNA preparations extracted from brain of mice infected with yellow fever virus (17D strain). The infected brains were homogenized with 0.85% sodium chloride to give a 10% homogenate, which was subjected to the cold 80% phenol method by Gierer and Schramm (1956).
Infectivity of the RNA preparations assayed in 7-day-old suckling mice was approximately 10^-3 of that of the original material. It was lost completely by 50μg/ml of RNA-ase within 10 minutes at 27°C, whereas DNA-ase exerted no effect; RNA-ase did not affect infectivity of the original materials. The viruses recovered from mice infected with the RNA were identified as the original yellow fever virus biologically and immunologically.
These data suggest that the infective principle in the RNA preparations is essentially the virus RNA itself.

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Hemagglutination inhibition (HI) tests with parainfluenza antigens were made on patients, chiefly adults, with acute respiratory illness.
1) Four-fold or greater monotypic rise in HI titer was obtained in 0.6, 0.7 and 4.1 per cent of the patients for types 1 (HA-2), 2 and 3 of parainfluenza virus, respectively. The serologic diagnosis could not be made with certainty in 3 cases because of cross-reactions.
2) Those cases showed upper-respiratory inflammation, bronchitis, pneumonitis or influenza-like illness and varied in severity.

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In the present paper are described the experimental evidences that some monosaccharides could inactivate the infectivity of certain purified phage particles. Since these phages are closely related with the somatic antigen O (12) of salmonella bacilli in their receptor or inactivating agent, the terminal sugar components of which have recently been clarified, there would be a possibility to analyse the configurational complementarity between the tail-tip of these phages and the antigenic determinant of this salmonella antigen through these specific inactivations by monosaccharides.
1) Phages a₁ and Pc have a close relationship with salmonella antigen O (12). The former, temperate phage, requires this antigen as the receptor for its adsorption and the latter, virulent phage, is easily inactivated by the agent closely related with this antigen.
2) According to the researches of Staub, Stocker and others, the determinant of this antigen is composed of the bifurcated oligosaccharide chain terminating with glucose and rhamnose, respectively. And the glucose chain has been known to have a sequence-α-glucose-galactose-mannose-rhamnose.
3) When mix-incubated with one molar solution of various mono- or di-saccharides at 37°C for one or three hours, the purified particles of these phages have been shown to be remarkably inactivated by some specific sugars.
4) So far examined, these two phages are proven to be inactivated only by D-glucose and D-mannose but not by D-galactose and L-rhamnose which also compose the determinant group of the O (12) antigen as well as the former two.
5) The inactivation rates observed in mix-incubation of Pc phage with one molar solution of D-glucose and D-mannose are respectively about 10^-6 and 10^-3, while those of a₁ phage with the same sugar solutions are just the reverse of the former indicating about 10^-3 with D-glucose and 10^-6 with D-mannose.
6) On the other hand, a₂ (temperate phage), T2, T4 and T3 (virulent phage of T series) which all have nothing to do with the O (12) antigen were examined, but the former three phages did not receive any influence from all tested sugars and only T3 was revealed to be inactivated by D-galactose and D-arabinose as well as D-glucose and D-mannose, though with lower rates than 10^-3.
7) Further more, several mono-, di- and trisaccharides were tested but all but melibiose have shown any detectable inactivating effects to these two phages.
All these experimental results were discussed in consideration of the complementarity which might exist between the molecular configuration of the tail-tip of a₁ and Pc phages and the terminal sugar components determining the specificity of salmonella O (12) antigen.

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When restricted ³²P-labeled phage infects the nonpermissive host, injected phage DNA is degraded more extensively and rapidly into acidsoluble components than in infection of the permissive host. It suggests that the specific degradation of phage DNA may be responsible for the restriction of phage growth in host-induced modification.
The breakdown of restricted phage DNA is prevented by heating the host cell prior to infection and the same treatment results in remarkable rise of EOP of restricted phage on nonpermissive host. (Toyama & Uetake, 1962, Toyama, 1963, Uetake et al., 1964)
These results indicate the presence of a thermolabile enzyme (DN-ase) which preexists in a host cell and degrades the restricted phage DNA soon after injection.

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