インフルエンザ・ウイルスのマウス感染症 (第6報)

経鼻感染と経腹腔感染の比較から眺めた抗体の感染症に対する参加の様式について

抄録

In the first paper of this series work, the inhibitory effect of the antibody produced at the time of primary infection on the virus growth at the late stage of infection was suggested. It was particularly the case at the time of intraperitoneal injection of a large amount of virus. In this study, detailed examinations were made on the growth characteristics of the same PR8 virus in lung after intranasal inhalation and again the effect of antibody on the virus growth was tested.
Seventh report following this paper will describe the production site of antibody against the PR8 virus and 8th paper may concern on the histopathological examination of the lung, particularly when the mice was infected intraperitoneally. When the descriptions in these series papers, from 6th to 8th, are taken together, significance or limitations of the immune mechanism to the development of infection will be revealed.
Main results obtained in this work will be summarized as follows:
1) Effect of the small amount of inoculum given by inhalation on the virus growth in lung and on the fate of mice was examined. As a result, 10^2.7 EID₅₀ particles were found to be necessary as the 50% lethal dosis. 10^1.2 EID₅₀ particles were necessary in inducing infections in 50% of the mice. Whenever the virus growth in lung was detectable, consolidation of the lung always followed.
2) At the time of intranasal infection, the initial antibody rise was fairly postponed when compared to that after intraperitoneal infection.
3) The decrease of virus titer in the lung exactly followed to the shift of serum antibody titer, when the small inoculum size was given by inhalation. This kind of keen correlation has been already secured at the time of intraperitoneal infection.
4) Virus growth at the time of intraperitoneal infection was also involved in the study to characterize the virus growth at the time of intranasal infections. Even when the large amount of virus was inoculated intraperitoneally, the inoculum actually participated in the multiplication in lung was estimated to be quite small and the initial rise in virus growth was postponed 6 hours when compared to the growth curve obtained at the time of inhalation.
5) Antibody response of mice receiving intraperitoneal injection of formaline-inactivated virus was also studied. On the basis of this observation, an experiment was conducted to see the participation of immune mechanism on virus growth. To do this, inactivated virus was injected intraperitoneally on the first day, then the sublethal amount of alive virus was inhaled on the second day. Growth of virus and consolidation of lung in these animals were almost similar to those obtained when the alive virus was given intraperitoneally. In other words, immunization effect of the formaline-killed virus given one day ahead was clearly demonstrated against the mice which received intranasal infection of small amount of virus.
6) To confirm the participation of viral antibody to the virus growth, radiation effect was studied with mice infected intranasally with small inoculum. With irradiated animals, virus growth continued longer than the non-irradiated.
Reviewing our experimental results as a whole, it is broadly true that the antibody response of the mice at the time of primary infection influences the virus growth in mouse lung, at late stage.