Immune response hampers lung repair after viral infections like COVID-19, study finds (Image credit: iStock)
A recent study has identified how immune cells hinder the repair of the lung’s protective barrier after viral infections such as COVID-19. This research, co-led by Cedars-Sinai and published in Nature, could lead to new therapeutic strategies aimed at improving lung recovery after infections. The results of the study shed light on why some patients suffer long-lasting complications, particularly lung scarring, after overcoming viral infections.
The COVID-19 pandemic has shown that viral infections can cause long-term health problems, a phenomenon now known as long COVID or post-acute sequelae of SARS-CoV-2 (PASC). Long COVID has left many patients incapacitated, with various symptoms even months after infection. Among the most serious complications are the post-acute sequelae of SARS-CoV-2 pulmonary fibrosis, a form of lung scarring that makes breathing difficult.
Patients with pulmonary fibrosis as a result of long COVID often experience extreme difficulty breathing, requiring oxygen supplementation and in some cases even lung transplants. With limited treatment options, many patients face long-term disability and life-threatening complications. Dr. Peter Chen, co-corresponding author of the study and interim chair of the Department of Medicine at Cedars-Sinai, explained, “Our study sought to understand the mechanisms behind abnormal lung repair that creates a scar-forming environment. These findings could pave the way for new treatments to prevent fibrotic lung disease after viral infections.”
The role of immune cells in preventing lung repair
Researchers developed models of post-viral lung disease and used molecular profiling and imaging to identify immune cells responsible for impeding lung regeneration. They identified a type of immune cell called CD8 T cells as a key factor in inhibiting lung healing after viral infections. These cells, which normally play a protective role by attacking infected cells, appear to create an environment that hampers the lungs’ ability to heal, leading to fibrosis.
The researchers analyzed data from patients with post-acute sequelae of SARS-CoV-2 pulmonary fibrosis. Their analysis confirmed that the abnormal immune pathways observed in animal models were also present in humans, reinforcing the link between immune response and lung damage after viral infections.
While this research focused on COVID-19, other viral pandemics, such as swine flu, have also demonstrated the potential to cause post-infection lung scarring. As co-author Dr. Jie Sun of the University of Virginia School of Medicine noted, “The medical community must be prepared to understand and prevent adverse outcomes from future viral outbreaks.” These findings offer valuable insight into the pathobiology of pulmonary fibrosis, with the potential to improve treatment for a variety of lung diseases caused by viruses.
This advance in understanding how immune responses impact lung repair could lead to the development of therapies that prevent long-term damage and improve recovery in patients affected by viral infections.
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