Respiratory Infections Such as COVID-19 Are Driving an Exponential Rise in Pulmonary Fibrosis Incidences
Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 24, 2025 8 hours, 13 minutes ago
Medical News: Viral infections leaving behind lasting scars in the lungs
Researchers from the University of Pennsylvania and the Children’s Hospital of Philadelphia have uncovered alarming evidence that common respiratory infections like COVID-19, influenza, and even latent viral infections such as Epstein-Barr virus can drive the onset of pulmonary fibrosis—a severe and often irreversible scarring of lung tissue. Once thought to be a rare condition, pulmonary fibrosis is now emerging as a hidden consequence of surviving viral respiratory illnesses. According to this
Medical News report, the findings highlight the urgent need to monitor patients long after recovery from infections.
Respiratory Infections Such as COVID-19 Are Driving an Exponential Rise in Pulmonary Fibrosis Incidences
What is pulmonary fibrosis and why it matters
Pulmonary fibrosis (PF) occurs when the lungs develop excessive scar tissue that interferes with normal breathing. Instead of healing properly after an infection or injury, the lung tissue becomes thick and stiff. This scarring makes it harder for oxygen to pass into the blood, leading to long-term breathing problems. Symptoms include shortness of breath, a persistent dry cough, fatigue, and reduced quality of life. Unlike typical recovery from infections, fibrosis can continue progressing long after the initial illness.
Evidence from COVID-19 and influenza survivors
The study revealed that as many as 70% of survivors of severe COVID-19–related ARDS (acute respiratory distress syndrome) showed fibrotic changes on their CT scans—compared to only 43% in non-COVID ARDS cases. Another large UK study estimated that around 11% of patients discharged after COVID-19 hospitalization still showed lung abnormalities months later, some indicative of fibrosis. Older age and prolonged use of ventilators were identified as additional risk factors. Influenza was also implicated, with roughly 25% of severe H1N1 patients developing fibrotic changes that persisted for months.
Dormant viruses adding to the risk
The research team also pointed out that viruses which remain dormant in the body, like Epstein-Barr virus (EBV) and cytomegalovirus (CMV), may reactivate and fuel chronic inflammation in the lungs. EBV has been detected in lung tissue from patients with idiopathic pulmonary fibrosis (IPF), suggesting that hidden viral activity could worsen scarring over time.
How the lungs are damaged
Pulmonary fibrosis after viral infection is caused by a “perfect storm” of immune system overreaction and disrupted repair processes. When the virus attacks lung cells, the immune system responds with inflammation. But instead of stopping when the infection is cleared, inflammation continues, leading to tissue damage. Specialized immune cells like macrophages and T cells can further drive scarring by releasing chemicals that activate fibroblasts, the cells responsible for depositing scar tissue. In severe cas
es, abnormal cell populations such as basaloid cells invade the lungs and worsen the scarring process.
Why this matters for the future
Unlike idiopathic pulmonary fibrosis, which usually progresses steadily and is often fatal, post-viral fibrosis can sometimes stabilize or even improve. However, it remains unpredictable, and for many patients the damage is permanent. Current antifibrotic drugs like pirfenidone and nintedanib slow disease progression but cannot reverse the damage. Scientists are now exploring therapies that target immune cell activity and fibroblast signaling to stop fibrosis before it becomes irreversible.
The researchers stress that as new viral outbreaks are inevitable, it is critical to recognize pulmonary fibrosis as a possible long-term complication. More attention must be given to monitoring patients after recovery and developing treatments that specifically address post-viral scarring.
The study findings were published in the peer reviewed American Journal of Physiology – Lung Cellular and Molecular Physiology
https://journals.physiology.org/doi/abs/10.1152/ajplung.00189.2025
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