Researchers at Weill Cornell Medicine have made a groundbreaking discovery on how SARS-CoV-2, the virus responsible for COVID-19, induces new cases of diabetes and exacerbates existing conditions. Published on September 2 in Cell Stem Cell, the study elucidates the mechanism by which the virus damages pancreatic cells crucial for insulin production.
Key Findings
The research team used advanced model systems to uncover the pathway through which SARS-CoV-2 triggers diabetes. Their findings highlight that the virus activates immune cells which, in turn, destroy beta (β) cells in the pancreas. These β cells are essential for producing insulin and regulating blood sugar levels.
Mechanism of Action
The study began with pancreatic tissue samples from COVID-19 patients who had died. Analysis revealed significant damage to the pancreatic islets, which are responsible for insulin production. Further investigation using a technique called GeoMx identified the presence of proinflammatory macrophages in the damaged tissues. These immune cells, intended to combat pathogens, inadvertently caused harm to the pancreatic cells.
To delve deeper, the researchers employed a novel model system developed in the Chen Lab: pancreatic islet organoids, miniature organs that include both a vascular system and immune cells. When infected with SARS-CoV-2, these organoids exhibited macrophage-induced cell death of β cells through a process known as pyroptosis.
Comparison with Other Viruses
The research also compared the effects of SARS-CoV-2 with another virus known for its association with type 1 diabetes, coxsackievirus B4. The organoids showed a similar macrophage response, suggesting that the underlying immune mechanism may be consistent across different viral infections.
Implications for Future Research
The findings could pave the way for developing clinical therapeutics aimed at preventing pancreatic damage in patients with severe COVID-19. While it is premature to test specific treatments, the research opens up possibilities for future interventions that might protect β cells during severe infections.
Additionally, the study’s insights into the role of immune signaling molecules may contribute to understanding long COVID, a condition affecting millions of people in the U.S. and potentially influencing diabetes outcomes.
Statements from Researchers
Dr. Shuibing Chen, co-corresponding author and director of the Center for Genomic Health, emphasized the significance of the discovery: “We were able to show how SARS-CoV-2 triggers diabetes by targeting pancreatic cells.”
Dr. Robert Schwartz, another co-corresponding author, noted the potential for future therapeutic development: “Moving forward, there may be a way to develop clinical therapeutics to avoid later injury to organs like the pancreas.”
The innovative use of pancreatic islet organoids in this study represents a significant advancement in understanding viral-induced diabetes and could have broad implications for both current and future research in the field.
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