Scientists from the University of California San Diego found that post-COVID lung disease shares origins with other scarring lung disorders.
The research was published in eBioMedicine and was conducted by Pradipta Ghosh et al.
While most people recover from COVID-19 within a week or two, up to one-third of survivors experience persistent or new symptoms weeks and months after initial infection.
One form of “long COVID” is interstitial lung disease (ILD), a group of chronic pulmonary disorders characterized by inflammation and scarring (fibrosis) that make it hard for the lungs to get enough oxygen.
Little is currently known about ILD, from diagnosis to prognosis to management. In its most severe form, the disease is fatal without a lung transplant.
In a new study, the team used an artificial intelligence (AI) approach.
They analyzed more than 1,000 human lung transcriptomic datasets associated with various lung conditions, specifically looking for gene expression patterns, inflammation signaling, and cellular changes.
The team found that lung fibrosis caused by COVID-19 resembles idiopathic pulmonary fibrosis (IPF), the most common and the deadliest form of ILD.
At a fundamental level, both conditions display similar gene expression patterns in the lungs and blood and dysfunctional processes within alveolar type II (AT2) cells.
AT2 cells play several critical roles in pulmonary function, including the production of lung surfactant that keeps lung cells from collapsing after exhalation and regeneration of lung cells after injury.
The authors were able to successfully induce these tell-tale elements in human lung organoids, in a hamster model of COVID-19, and could confirm their presence in the lungs of deceased individuals with COVID-19.
Key elements were also reversed in the hamsters using anti-SARS-COV-2 therapeutics. A deeper analysis pinpointed endoplasmic reticulum stress as the shared early trigger of both post-COVID lung disease and ILD.
The team says the insights, biomarkers, tools, mechanisms, and promising therapeutic avenues identified here are likely to spur the development of therapies for patients with IPF and other fibrotic interstitial lung diseases, all of whom have limited or no treatment options.
If you care about COVID, please read studies about how COVID-19 damages lungs, and aspirin could help prevent COVID-19 deaths.
For more information about COVID, please see recent studies about new COVID vaccine for people with weak immune systems, and results showing exposure to harmless coronaviruses can boost your COVID-19 immunity.
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