Hospitalizations and deaths from COVID-19 are on the decline following a winter wave of XBB.1. 5, a recent Omicron subvariant–but we’re not out of the woods just yet. Scientists are warning of a possible “second wave” in pandemic deaths from long-term COVID conditions like lung scarring, which causes damage to tissue and blood vessels, as well as the air sacs and small blood vessels within the lungs.
Scarring leads to a permanent inability for the lungs to carry oxygen and can lead to heart failure if severe. Many questions remain about why certain patients develop this condition, called lung fibrosis, and whether it can be prevented and reversed before they require lung transplants.
Luckily, there’s new hope. 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. The study was published on Feb. 27 in the Proceedings of the National Academy of Sciences.
“This represents a much-needed model of post-viral induced lung fibrosis that is highly relevant to fibrotic lung diseases,” Harry Karmouty-Quintana, a pulmonary disease researcher at The University of Texas Health Science Center at Houston who was not involved in the research, told The Daily Beast. He said that understanding the severity of cases could assist pulmonologists in identifying and treating these patients.
While rare, over 200 lung transplants had been performed in the U.S. for severe, irreversible lung damage caused by COVID-19. And unlike other conditions that can require a lung transplant in years or decades, a December study found that long COVID can cause a person’s condition to deteriorate in months.
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.
Genetics likely plays a prominent role in this condition, Karmouty-Quintana said. In order to repair damaged cells, a set of genes is responsible. However, in cases like Idiopathic Pulmonary Fibrosis (which has been better studied), it is the excessive activity of some genes that can cause harmful scarring.
In this new study, researchers sequenced five lung samples of patients with COVID who had to have lung transplants. They also compared the sequencing results to lung samples taken from people who died unrelatedly. The form of sequencing they used allowed them to quantify the activity of different genes. They found that long COVID-associated Fibrosis was caused by overactivation in the innate immune system. This is the body’s initial response to infection and can cause widespread, nonspecific inflammation to try to incapacitate the invader. Next, they created mice with human lung organoids. These are three-dimensional clusters made up of cells from humans. They then infected these mice with an engineered version of SARS-CoV-2 and gave them a drug that damaged their lungs to recreate a mouse model of long COVID fibrosis. The researchers then treated the mice using a mixture of two antibodies that block genes related to innate immunity to reduce the risk of lung scarring.
Four weeks later, the fibrosis in the mice treated with antibodies was reversed. The mice had lungs that looked and worked like untreated ones. These antibodies could represent potential therapeutic targets, the authors wrote, though future tests in humans are needed.
Karmouty-Quintana said that additional studies should look at rats, which are considered the field’s standard when it comes to respiratory viruses. Additionally, these findings could inform research into chronic respiratory problems stemming from other viral infections, as these, too, have been associated with the innate immune system. He stated that the ultimate goal would be to stop lung scarring from becoming irreversible.
“There is an opportunity to intervene with treatments before patients progress to fibrosis–I think that’s exciting,” he said.
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