Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 19 (COVID-19), a global pandemic that originated in Wuhan, China, at the end of 2019 and has resulted in over 6 million deaths to date (according to WHO, as of March 2022). Overall, SARS-CoV-2 had diminished potential to replicate, affect morphology and evoke immune responses in bronchial epithelial cells compared to H1N1. We did not find any differences in the epithelial response to SARS-CoV-2 infection between paediatric and adult cells. Interestingly, H1N1 infection resulted in sustained upregulation of SARS-CoV-2 entry factors FURIN and NRP1.
Only H1N1 infection caused disruption of the epithelial layer. While infection with either virus triggered robust transcriptional interferon responses, including induction of type I ( IFNB1) and type III ( IFNL1) interferons, markedly lower levels of interferons and inflammatory proteins (IL-6, IL-8) were released following SARS-CoV-2 compared to H1N1 infection. We investigated viral replication and immune responses in SARS-CoV-2-infected bronchial epithelial cells from healthy paediatric ( n = 6 2.5–5.6 years old) and adult ( n = 4 47–63 years old) subjects and compared cellular responses following infection with SARS-CoV-2 or Influenza A H1N1.
Airway epithelial cells play a vital role in the early defence against viruses via their barrier and immune functions. Children are less likely than adults to suffer severe symptoms when infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), while influenza A H1N1 severity is comparable across ages except for the very young or elderly.
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