The bulletin of the Yamaguchi Medical School

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The bulletin of the Yamaguchi Medical School Volume 22 Issue 1
published_at 1975-03

Immunohistopathological and Electron Microscopical Studies on Influenza Virus Multiplication in Hatching Egg and on Pathogenesis of Experimental Influenza Pneumonia

Immunohistopathological and Electron Microscopical Studies on Influenza Virus Multiplication in Hatching Egg and on Pathogenesis of Experimental Influenza Pneumonia
Aoyama Sakae
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Influenza virus A/Tokyo/1/72 (10^7.5 EID_50) was inoculated into CAC of the hatching egg for examinating of the virus multiplication, and intranasally into murine lung for study of pathogenesis of influenzal pneumonia. These studies were investigated by immunofluorescent, histological and electron microscopical appearances. In the hatching egg, difference of susceptibility to influenza virus was observed between entoderm and ectoderm. On immunofluorescent study, IF was detected not only in CAM but also in the other membranes and rarely in embryo, especially in respiratory epithelium. In the murine lung, influenza virus invaded to tracheal and bronchial epithelium and finally to type II pneumocyte of alveolar lining cells. These facts suggested that influenza virus had intense respiratory epitheliotrop ism. In the murine lung, cytoplasmic IF was observed at 9 hours after inoculation in epithelium of trachea and bronchiole at first, and at 12 hours after inoculation, scattered IF in some alveolar wall, and at 1 day after inoculation in nuclei of desquamated epithelial cells in the lumen of the trachea and bronchial tube. IF was most brilliant between 1 to 3 days after inoculation. But in the light microscopic study, most violent histological changes were detected at 2 and 10 days after inoculation. Therefore, there was a difference in time between IF intensity and histolgical changes. About the pathogenesis of viral pneumonia in this study, many inflammatory cells infiltrated around the trachea, bronchial tube and to alveolar wall, however IF could not be noticed among them. Consequently, it was speculated that interstitial pneumonia might be a reaction caused by some toxic substance resulted from influenza virus in infected cells. So, influenzal pneumonia was seemed to be secondary reaction due to influenza virus infection.