A new study led by Stanford University researchers highlights an underlying genetic cause for long COVID fibrosis—and was able to prevent it from developing in mice.
Treating this condition “poses a significant challenge to global health,” the authors write in the new study. But doing so, they add, is “essential to prevent a second wave of late mortality associated with this pandemic” among people with fibrosis due to COVID-19.
In the new study, the researchers genetically sequenced lung samples taken from five long COVID patients who required lung transplants and compared them to sequencing done on lung samples from controls of people who died from unrelated causes. The form of sequencing they used allowed them to quantify the activity of different genes.
Four weeks later, the antibody-treated mice’s fibrosis reversed, restoring their lungs to normal appearance and function compared to untreated mice. These antibodies could represent potential therapeutic targets, the authors wrote, though future tests in humans are needed.
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