Experimental infection of herpesvirus cuniculi (HCV or Virus III) was studied as a model of latent infection of herpes group virus.
The growth of HCV in rabbit kidney (RK) cell cultures was rather slow when the cells were infected at a multiplicity of approximately 10. Infective virus appeared 30 hours after infection, and a maximum titer of 10⁶ TCID₅₀/0.2ml reached on the 4th day. The infectivity titer of cellassociated virus was 2 log TCID₅₀ higher than that of fluid virus.
When HCV was inoculated intracutaneously or intravenously into a rabbit, it began to be detected from peripheral leukocytes on the 7th day after infection. It was isolated constantly from leukocytes over a period of at least 14 months. Concurrently, neutralizing and complement-fixing antibodies were demonstrated in the serum.
To detect infective virus, leukocytes were cultivated with RK cells. The number of leukocytes needed for positive virus isolation ranged from 800 to 100, 000, depending on the species of animals and/or the time of bleeding. No virus could be recovered from fresh leukocytes which had been disrupted by freezing and thawing before inoculated onto RK cells. It was recovered, however, when RK cells were inoculated with leukocytes which had been incubated in vitro at 37°C for two days prior to the occurrence of disruption by freezing and thawing. These results suggest that the virus may have existed in an inactive from in fresh leukocytes, that it may have been converted in to an infective form in these leukocytes when cultivated in vitro, and that it may have multiplied most efficiently in RK cells.
Virus was also recovered from leukocytes obtained from various organs, such as brain, lung, spleen, kidney, liver, and uterus, of rabbits which were infected with the virus 4, 6 or 14 months before and cultivated with RK cells.
In order to demonstrate that a rabbit was infected with HCV, it was a most sensitive method to isolate the virus from peripheral leukocytes cultivated with RK cells. The demonstration of neutralizing and/or complement-fixing antibodies was also useful for the same purpose. Serological surveillance of 101 rabbits obtained in the Tokyo area failed to show the production of any specific antibody against HCV.

抄録全体を表示

Herpes simplex virus (HSV) is reported to be relatively insensitive to the antiviral activity of interferon (IF), but no detailed information is available for it.
To obtain basic data on the clinical application of IF to human beings, studies were made on the effect of IF against the newly isolated HSV, HSV-TM strain, both in the tissue culture system of mouse embryo cells and in the mouse system with animals suffering from skin eruption and encephalitis.
1) Fifty per cent inhibition of the cytopathic effect, or virus yield, was observed when mouse embryo cells were treated with 10 units of IF and challenged with 50 TCID₅₀ of HSV-TM strain. A complete inhibition was seen when mouse embryo cells were treated with 100 units of IF and challenged with 5, 000 TCID₅₀ of HSV-TM.
2) Hairless mice of the 88-k strain were treated intraperitoneally with IF 24 hours before viral inoculation and daily thereafter. Daily inoculation with concentrated mouse IF, the maximum titer of which was 1.7×10⁵IU/0.3ml, did not inhibit the development of skin eruption in mice inoculated subcutaneously with 0.2ml of HSV-TM (10^5.5TCID₅₀/ml or encephalitis in mice inoculated intracerebrally with 0.03ml of HSV-TM (30 TCID₅₀).
These results imply that the administration of larger doses of interferon may be required for prophylaxis or treatment of HSV infection in animals.

抄録全体を表示

Green monkey kidney cell (GMK) cultures were used to compare some biological properties between the prototype strain Cox. A-16 and strain 69-70, a representative strain which had been isolated from vesicular fluids of patients with hand-foot and mouth disease (HFMD). Some marker-tests of poliovirus were also applied tentatively to both strains. The results obtained are summarized as follows.
Strain 69-70 showed a resistance to anti-69-70 and anti-Cox. A-16 serum, but the prototype strain was readily neutralized by both sera. This character was not alterd by cells used in experiments for virus isolation, multiplication, and neutralization.
The infectivity of the prototype strain was 2 log units higher than that of strain 69-70. Electron microscopic observation suggested that many empty virions of strain 69-70 might have been produced.
There was a marked reduction in the plaque size and the efficiency of plating of the prototype strain under an acidic agar-overlay, whereas strain 69-70 was not affected with a wide range of bicarbonate concentration.
Heating at 50°C in the presence of AlCl₃ was effective for stabilizing the infectivity of the prototype strain, but had no such significant effect on that of strain 69-70.
The effect of temperature on viral growth of both strains was examined in titration of infective virus at 40, 37, and 30°C. The prototype strain grew readily at these temperatures, but the growth of strain 69-70 was repressed under the same experimental conditions.
From the results obtained, it was suggested that the epidemic of HFMD occurring in Japan over a period from 1969 to 1970 might have been induced by the invasion of a new variant strain of Cox. A-16 virus.

抄録全体を表示