Cells That Survive Acute SARS-CoV-2 Infection Play a Role in Lung Inflammation and Recovery
Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 02, 2025 1 month, 2 days, 18 hours, 22 minutes ago
Medical News: A team of researchers from the University of Iowa-USA has made significant discoveries about how certain lung cells survive acute SARS-CoV-2 infection and play a role in both inflammation and lung regeneration. Their findings provide a new understanding of the aftermath of severe COVID-19 cases, particularly how the body recovers and why some patients experience long-term symptoms. This
Medical News report explains the study’s key findings and their potential implications for post-COVID conditions.
Cells That Survive Acute SARS-CoV-2 Infection Play a Role in Lung Inflammation and Recovery
The Role of Surviving Cells in COVID-19 Recovery
COVID-19 has led to millions of infections worldwide, with many survivors continuing to suffer from long-term health issues. Researchers have now focused on understanding what happens to lung cells that survive the acute phase of infection. They found that a specific type of lung cell, called alveolar epithelial cells, can persist after the infection and contribute to both immune responses and lung recovery.
Using advanced experimental models in mice, scientists tracked these surviving cells over time. They found that while many infected cells die, some remain and become active participants in the lung’s healing process. However, these cells also seem to contribute to prolonged inflammation, which could explain why some COVID-19 patients suffer from persistent respiratory issues long after recovering from the initial infection.
Study Methodology and Findings
To examine the behavior of these surviving cells, researchers used genetically modified mice that allow scientists to track infected cells even after they are no longer carrying live virus. They utilized two different mouse models:
-Mice infected with a highly virulent strain of SARS-CoV-2 - In these mice, researchers found that alveolar type 2 (AT2) cells, which are crucial for lung repair, survived the infection. These cells transformed into a transitional cell type associated with lung regeneration.
-Mice infected with a milder strain - In these cases, researchers observed that alveolar type 1 (AT1) cells, which are responsible for oxygen exchange, were able to survive. The presence of these cells allowed for faster lung recovery and less severe long-term effects.
One of the study’s significant discoveries was that in the case of severe infections, the surviving AT2 cells exhibited signs of prolonged activation and incomplete differentiation. This means that while they attempted to repair the lung, they did not fully transform into functional AT1 cells. This incomplete transition may lead to persistent lung inflammation and fibrosis, which is common in long COVID cases.
Implications for Long COVID and Lung Health
These findings have important implications for understanding post-COVID-19 complications. Many COVID-19 survivors report lingering respiratory symptoms such as shortness of bre
ath and fatigue, often referred to as post-acute sequelae of COVID-19 (PASC) or long COVID. The study suggests that the prolonged presence of these surviving but dysfunctional lung cells could be a key factor contributing to these long-term symptoms.
The researchers also observed increased interactions between surviving lung cells and immune cells. Specifically, they found that immune cells remained active around the surviving AT2 cells for extended periods. This prolonged immune activation might lead to continued lung inflammation, potentially worsening respiratory health over time.
What This Means for Future Treatments
Understanding how SARS-CoV-2 affects lung cells opens new possibilities for treatment. If scientists can find ways to accelerate the proper differentiation of AT2 cells into functional AT1 cells, they may be able to reduce long-term lung damage in COVID-19 patients. Potential therapies could focus on:
-Reducing chronic inflammation - Finding ways to limit prolonged immune activation in the lungs may help ease long COVID symptoms.
-Boosting lung cell repair mechanisms - Enhancing the proper transition of AT2 cells into AT1 cells could improve lung function after infection.
-Targeting lingering infected cells - Developing treatments that can effectively clear these surviving cells or regulate their activity could be crucial in preventing long-term lung complications.
Conclusion
This study provides crucial insights into how some lung cells survive acute SARS-CoV-2 infection and their role in both inflammation and lung regeneration. While the surviving cells help in repairing lung tissue, they also contribute to prolonged immune responses, which might explain persistent respiratory issues in long COVID patients. The findings highlight the need for further research into therapeutic approaches that can enhance lung recovery while minimizing chronic inflammation. These discoveries bring us one step closer to developing treatments that could help millions of people suffering from the long-term effects of COVID-19.
The study findings were published in the peer-reviewed journal: mBio.
https://journals.asm.org/doi/10.1128/mbio.03693-24
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