A mouse model was established for the study of acute myocarditis that occurs during influenza infection. Challenge with more than 10 LD50 of mouse‐adapted influenza A2 virus (H2N2) induced myocarditis macroscopically discernible as white, irregularly shaped lesions which were shown by histological examination to consist of necrotic myofibers surrounded by infiltrating mononuclear inflammatory cells. After challenge with 10 LD50 of the virus, macroscopic myocarditis was found to advance in a progressive manner up to the 7th day, while the virus titer in the heart reached its peak on the 2nd day and began to decrease on the 5th day of infection. However, development of myocarditis was significantly suppressed in mice which were irradiated with 400 R of X‐rays before infection. In addition, myocarditis did not develop in congenitally athymic nude mice. These data indicate that myocarditis was not brought about by viral action directly, but that it was mediated by some function of the host against viral in‐vasion, which was abolished by X‐irradiation. The data also suggest that T cells played a key role in the development of myocarditis.
|Original language||English (US)|
|Number of pages||9|
|Journal||MICROBIOLOGY and IMMUNOLOGY|
|State||Published - Feb 1981|
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