tetano
Editor, Senior Moderator
Am J Pathol. 2019 Dec 19. pii: S0002-9440(19)30861-2. doi: 10.1016/j.ajpath.2019.11.003. [Epub ahead of print] [h=1]Distinct chronic post-viral lung diseases upon infection with influenza or parainfluenza viruses differentially impact superinfection outcome.[/h]
Garcia GL[SUP]1[/SUP], Valenzuela A[SUP]1[/SUP], Manzoni T[SUP]1[/SUP], Vaughan A[SUP]2[/SUP], L?pez CB[SUP]3[/SUP].
[h=3]Author information[/h] 1 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. 2 Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States; Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States. 3 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. Electronic address: lopezca@upenn.edu.
[h=3]Abstract[/h] Chronic obstructive pulmonary disease (COPD) and asthma remain prevalent human lung diseases. Variability in both epithelial and inflammatory components resulting in pathology heterogeneity complicate the development of treatments for these diseases. Early childhood infection with parainfluenza virus or respiratory syncytial virus strongly associates with the development of asthma and COPD later in life and exacerbations of these diseases correlate with the presence of viral RNA in the lung. Well-characterized animal models of post-viral chronic lung diseases are necessary to study the underlying mechanisms of viral-related COPD and asthma and to develop appropriate therapies. In this study, we cross-analyzed chronic lung disease caused by infection with Sendai virus (SeV) or influenza A virus in mice. Differences wee observed in both lesion composition and inflammatory profiles between SeV- and influenza A virus-induced long-term lung disease. In addition, a primary SeV infection led to worsened pathology upon secondary heterologous viral challenge while the reversed infection scheme protected from disease in response to a secondary viral challenge more than a month after the primary infection. These data demonstrate the differential impact of primary viral infections in the susceptibility to disease exacerbation in response to a different secondary viral infection and highlight the usefulness of these viral models as tools to understand the underlying mechanisms mediating distinct chronic post-viral lung diseases.
Copyright ? 2019. Published by Elsevier Inc.
PMID: 31866346 DOI: 10.1016/j.ajpath.2019.11.003
Garcia GL[SUP]1[/SUP], Valenzuela A[SUP]1[/SUP], Manzoni T[SUP]1[/SUP], Vaughan A[SUP]2[/SUP], L?pez CB[SUP]3[/SUP].
[h=3]Author information[/h] 1 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. 2 Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States; Institute for Regenerative Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States. 3 Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, United States. Electronic address: lopezca@upenn.edu.
[h=3]Abstract[/h] Chronic obstructive pulmonary disease (COPD) and asthma remain prevalent human lung diseases. Variability in both epithelial and inflammatory components resulting in pathology heterogeneity complicate the development of treatments for these diseases. Early childhood infection with parainfluenza virus or respiratory syncytial virus strongly associates with the development of asthma and COPD later in life and exacerbations of these diseases correlate with the presence of viral RNA in the lung. Well-characterized animal models of post-viral chronic lung diseases are necessary to study the underlying mechanisms of viral-related COPD and asthma and to develop appropriate therapies. In this study, we cross-analyzed chronic lung disease caused by infection with Sendai virus (SeV) or influenza A virus in mice. Differences wee observed in both lesion composition and inflammatory profiles between SeV- and influenza A virus-induced long-term lung disease. In addition, a primary SeV infection led to worsened pathology upon secondary heterologous viral challenge while the reversed infection scheme protected from disease in response to a secondary viral challenge more than a month after the primary infection. These data demonstrate the differential impact of primary viral infections in the susceptibility to disease exacerbation in response to a different secondary viral infection and highlight the usefulness of these viral models as tools to understand the underlying mechanisms mediating distinct chronic post-viral lung diseases.
Copyright ? 2019. Published by Elsevier Inc.
PMID: 31866346 DOI: 10.1016/j.ajpath.2019.11.003