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SARS-CoV-2 (COVID-19) Adhesion Site Protein Upregulation in Small Airways, Type 2 Pneumocytes, and Alveolar Macrophages of Smokers and COPD - Possible Implications for Interstitial Fibrosis.

Samuel James BrakeMathew Suji EapenKielan Darcy McAlindenJames MarkosGreg HaugJosie LarbyCollin ChiaAshutosh HardikarGurpreet Kaur SingheraTillie L HackettWenying LuSukhwinder Singh Sohal
Published in: International journal of chronic obstructive pulmonary disease (2022)
The increased expression of ACE2, TMPRSS2 and Furin, in the SAE, type 2 pneumocytes and AMs of smokers and COPD are detrimental to lung function and proves that these patient groups could be more susceptible to severe COVID-19 infection. Increased type 2 pneumocytes suggest that these patients are vulnerable to developing post-COVID-19 interstitial pulmonary fibrosis or fibrosis in general. There could be a silently developing interstitial pathology in smokers and patients with COPD. This is the first comprehensive study to report such changes.
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