{'fraction_non_alphanumeric': 0.023098591549295774, 'fraction_numerical': 0.024225352112676058, 'mean_word_length': 5.3428571428571425, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Alterations in pulmonary ultrastructure and morphometric parameters induced by parainfluenza (Sendai) virus in rats during postnatal growth.

The ultrastructural and morphometric effects of viral respiratory disease during postnatal lung growth were examined in weanling (22-day-old) and suckling (5-day-old) rats infected with parainfluenza Type 1 (Sendai) virus. Viral nucleocapsids and budding virions were identified by transmission electron microscopy in ciliated cells, mucous cells, and nonciliated bronchiolar epithelial cells of weanling rats at 5 days after inoculation and were associated with epithelial necrosis and erosion as well as hyperplasia of nonciliated bronchiolar epithelial cells. Interstitial pneumonia characterized in early stages by swelling and sloughing of Type 1 and Type 2 alveolar epithelial cells was also present at 5 and 7 days after inoculation. Lesions persisting at 30, 60, and 90 days after inoculation included multifocal connective tissue polyps in terminal bronchioles that partially obstructed bronchiolar lumens. Specific lung volume was greater (P less than 0.01) in weanling rats at 30 and 60 days following viral infection than in control rats, and specific alveolar surface area was 42% greater (P less than 0.01) in infected rats at 60 days after inoculation. Suckling rats infected during a phase of rapid postnatal lung growth at 5 days of age had 33% greater (P less than 0.02) specific alveolar surface area and 48% greater (P less than 0.001) mean terminal bronchiolar cross-sectional area when compared with control rats at 22 days of age. The results indicate that viral pulmonary infection during early life can induce acute and persistent alterations in pulmonary structure that could adversely affect lung function.