The surprising link between SARS-CoV-2 infection and new-ons
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In this study, researchers analyzed datasets of gene expression from patients, as well as in vivo and in vitro models, infected with SARS-CoV-2. They specifically looked for genes that were noticeably over- or under-expressed compared with uninfected patients, animals, or cells. Infection with SARS-CoV-2 affected the expression of insulin/IGF signaling pathway components in the lung, liver, adipose tissue, and pancreatic cells. Moreover, these changes were attributed in part to activation of interferon regulatory factor 1 (IRF1). Further investigation showed that IRF1 expression is elevated in older patients, men, obese individuals, and patients with diabetes. The synergistic effect of older age, male sex, obesity and diabetes with SARS-CoV-2 means that the expression of IRF1 occurs at an increased rate, which may explain why these patients are more vulnerable to COVID-19. In addition, critical patients with COVID-19 had higher IRF1 expression and lower insulin/IGF signaling pathway genes in their blood compared with noncritical patients. Finally, treating SARS-CoV-2–infected cells or an animal model with hormonal factors that decreased IRF1 expression enhanced insulin/IGF signaling. Our findings suggest that SARS-CoV-2 infection impairs insulin/IGF signaling by increasing IRF1 expression, thereby disrupting blood sugar metabolism. Decreasing IRF1 expression by treatment with factors such as dihydrotestosterone and dexamethasone could help mitigate the effects of COVID-19.

Source: https://linkinghub.elsevier.com/retrieve/pii/S0026049522001147
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