COVID-19 resembles IPF at a fundamental level
In the aftermath of COVID-19, a significant number of patients develop a fibrotic lung disease, for which insights into pathogenesis, disease models, or treatment options are lacking, according to researchers Sinha and colleagues. This long-haul form of the disease culminates in a fibrotic type of interstitial lung disease .
The lung transcriptomic datasets compared in their study were associated with various lung conditions. The researchers used two viral pandemic signatures and one COVID lung-derived signature. They found that the resemblances included that COVID-19 recapitulates the gene expression patterns , cytokine storm , and the AT2 cytopathic changes, eg, injury, DNA damage, arrest in a transient, damage-induced progenitor state, and senescence-associated secretory phenotype .
PPI-network analyses pinpointed endoplasmic reticulum stress as one of the shared early triggers of both IPF and COVID-19, and immunohistochemistry studies validated the same in the lungs of deceased subjects with COVID-19 and the SARS-CoV-2-challenged hamster lungs. Additionally, lungs from transgenic mice, in which ER stress was induced specifically in the AT2 cells, faithfully recapitulated the host immune response and alveolar cytopathic changes that are induced by SARS-CoV-2.
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