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Alterations in pulmonary ultrastructure and morphometric parameters induced by parainfluenza (Sendai) virus in rats
Insights
Viral respiratory infections in young rats during early lung development cause lasting structural changes. These alterations, including increased lung volume and alveolar surface area, may negatively impact lung function long-term.
Area of Science:
- Pulmonary pathology
- Developmental biology
- Virology
Background:
- Postnatal lung development is crucial for respiratory health.
- Viral infections can disrupt normal lung growth and function.
Purpose of the Study:
- To investigate the ultrastructural and morphometric effects of parainfluenza Type 1 virus infection on postnatal rat lung growth.
- To assess acute and persistent pulmonary alterations induced by early-life viral infection.
Main Methods:
- Weanling (22-day-old) and suckling (5-day-old) rats were infected with parainfluenza Type 1 (Sendai) virus.
- Transmission electron microscopy was used to identify viral presence and cellular damage.
- Morphometric analysis evaluated lung volume, alveolar surface area, and bronchiolar dimensions at various time points post-infection.
Main Results:
- Viral nucleocapsids and virions were observed in epithelial cells, associated with necrosis and hyperplasia.
- Persistent lesions included connective tissue polyps obstructing bronchiolar lumens.
- Infected weanling rats showed increased specific lung volume and alveolar surface area.
- Suckling rats infected early exhibited significantly greater specific alveolar surface area and terminal bronchiolar cross-sectional area.
Conclusions:
- Viral pulmonary infections during early life induce acute and persistent structural changes in the developing lung.
- These alterations, including increased lung volume and surface area, may lead to adverse long-term effects on lung function.
- The findings highlight the vulnerability of the developing lung to viral insults.
Abstract:
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.