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Throughout the COVID-19 pandemic, doctors have noted that some patients are at particular risk of developing severe cases or dying from coronavirus infection.
Type 2 diabetes is one of the main risk factors for severe Covid-19 disease. New research from the University of Michigan reveals why this is happening and offers hope for a possible cure.
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The culprit appears to be an enzyme called SETDB2. This same enzyme is involved in non-healing inflammatory wounds found in diabetic patients.
Working in the lab of Catherine Gallagher, MD, in the Michigan Departments of Surgery, Microbiology and Immunology, researcher W. James Melvin and his colleagues set out to study the potential link between the enzyme and inflammation endemic that they themselves saw in COVID-19 intensive care unit patients.
And in a mouse model infected with the coronavirus, they found that SETDB2 was decreased in immune cells involved in the inflammatory response, called macrophages, in diabetic mice. They later saw the same in the blood of single-celled macrophages from patients with diabetes and severe Covid-19.
“We think we have a reason why these patients developed a cell storm,” Melvin said.
In mouse and human models, Melvin and Gallagher note that with a decrease in SETDB2, inflammation increased. In addition, they revealed that a pathway known as JAK1 / STAT3 regulates SETDB2 in macrophages during MERS infection.
Taken together, the results suggest a potential treatment route. Previous lab results have shown that interferon, a cytokine important for viral immunity, increases SETDB2 in response to wound healing.
In their new study, they found that serum from intensive care unit patients with diabetes and severe “Covid-19” reduced levels of interferon beta compared to patients without diabetes.
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“Interferon has been studied throughout the pandemic as a potential treatment, with efforts between trying to increase or decrease interferon levels,” Gallagher said. “My feeling is that its effectiveness as a treatment will be both patient and time specific.”
To test this, the study team administered beta interferon to mice infected with the coronavirus and found that it was able to increase SETDB2 and reduce inflammatory cytokines.
Melvin and Gallagher hope the results of this study will benefit ongoing clinical trials of interferon or other components of the pathway, including epigenetic targets, for “Covid-19”. Their work also emphasizes the need to understand the timing and specificity of cells in therapy and to tailor its application to the underlying conditions of patients, especially those with diabetes.
“Our research shows that it could actually make a big difference if we could target diabetic patients who have interferon, especially early in the infection,” Melvin said.
Source: Medical Express
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