We read with great interest the study by Lyu et al. (1), recently published in Diabetes, which integrated Mendelian randomization with an H1N1-infected diabetic mouse model to link type 2 diabetes (T2D) to reduced interferon-α2 (IFN-α2) and impaired antiviral defense. The authors showed a negative genetic association between T2D and IFN-α2 levels and further demonstrated that exogenous IFN-α2 improved survival, reduced viral burden, attenuated lung injury, and suppressed JAK/STAT3-associated inflammation in db/db mice. These findings provide an important mechanistic bridge between metabolic disease and severe respiratory viral infection.
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