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Sequential virus infections, bacterial superinfections, and fibrogenesis
1Department of Environmental Health Sciences, Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland 21205.
Abstract:
Parainfluenza 1 (Sendai) and influenza A virus pneumonitis cause severe lung damage, which, upon resolution, is followed by persistent alveolitis and parenchymal changes characterized by patchy consolidation and collagen deposition in the affected areas. To determine whether these long-term sequelae of the virus pneumonias are cumulative, mice were infected by aerosol inhalation with Sendai virus, influenza A virus, or Sendai followed 30 days later by influenza virus infection. At 90 days after the initial infection, mice were killed for assay of long-term parenchymal changes as quantitated lung hydroxyproline (Hpr) content, morphometric analysis, and total and differential lavage cell counts. Sendai virus infection did not alter the proliferation of influenza virus in the lungs as quantitated by infectious virus titers on Day 1, 3, 5, 7, 9, and 11 of influenza infection. At Day 90, lung Hpr content was cumulative in dual-infected mice, with a concomitant increase in the persistent alveolitis. To determine whether bacterial infections played a similar role in these long-term pulmonary sequelae, mice were infected by aerosol inhalation with either Staphylococcus aureus or Klebsiella pneumoniae or, during the course of influenza virus infection, superinfected with each of the bacteria. Sixty days after infection with K. pneumoniae alone, lung Hpr levels were significantly increased over those in noninfected control mice. Infection with S. aureus had no effect on the quantitated parameters of long-term lung damage. In influenza-infected mice superinfected with K. pneumoniae, lung Hpr content was significantly increased over that of S. aureus did not elevate any quantitated parameter of lung damage when compared with the virus alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Insights
Dual viral pneumonia infections in mice lead to cumulative lung damage and persistent alveolitis. Bacterial superinfections, particularly Klebsiella pneumoniae, exacerbate these long-term pulmonary effects.
Area of Science:
- Pulmonary Medicine
- Virology
- Immunology
Background:
- Parainfluenza 1 (Sendai) and influenza A virus cause lung damage, leading to persistent alveolitis and collagen deposition.
- The cumulative nature of these long-term sequelae following viral pneumonias requires further investigation.
Purpose of the Study:
- To determine if long-term lung damage from viral pneumonias is cumulative.
- To investigate the role of bacterial superinfections in exacerbating viral-induced pulmonary sequelae.
Main Methods:
- Mice were infected with Sendai virus, influenza A virus, or sequentially with both.
- Lung hydroxyproline (Hpr) content, morphometric analysis, and lavage cell counts were used to assess long-term parenchymal changes.
- Mice were also infected with Staphylococcus aureus or Klebsiella pneumoniae alone or superinfected during influenza virus infection.
Main Results:
- Dual Sendai and influenza A virus infections resulted in cumulative lung hydroxyproline content and increased persistent alveolitis at 90 days.
- Klebsiella pneumoniae infection alone significantly increased lung Hpr levels.
- Superinfection with K. pneumoniae during influenza A virus infection further elevated lung Hpr content, while S. aureus had no significant effect.
Conclusions:
- Long-term lung damage from sequential viral pneumonias is cumulative.
- Klebsiella pneumoniae superinfection significantly exacerbates virus-induced lung damage, suggesting a role for bacterial co-infections in chronic pulmonary disease progression.