Abstract
In human beings and in experimental animals, influenza virus causes a cytonecrosis in the ciliated respiratory epithelium. This results in an epithelial wound which facilitates secondary infection with respiratory pathogens, including the dangerous groups of pyogenic cocci. During the pandemic of Asian influenza (1957-1958) many people died from a curious form of pneumonia without coexistent bacterial infection. The histopathology resembles closely some of the descriptions of fatal 1918 influenzal pneumonia. The same type of pneumonia was seen in the winter of 1960. Microscopic analysis of those cases shows that it is very probable that the virus attacks the alveolar cell lining, subsequently causing its destruction. The vascular damage is considered to be a phenomenon secondary to the destruction of this lining. Experimental influenza virus pneumonia in mice is basically the same process. Unknown host factors favoring the development of influenza virus pneumonia most probably do exist. So far, it is not certain that the Asian virus of 1957 has manifested an enhanced genetic human pneumotropic virulence.
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