Frontiers in Virology · Published 2026-03-25 · DOI 10.3389/fviro.2026.1751938
IntroductionCoronavirus infection in humans may cause not only pulmonary infection but also secondary intestinal infection. The AKT inhibitors have a significant inhibitory effect on various coronavirus infections, and they can effectively alleviate the intestinal barrier damage induced by the SARS-CoV-2. However, it is unknown how the AKT inhibitors exert their anti-viral effects through the intestinal tract.MethodsHCoV-OC43-infected mice were treated with MK-2206 or vehicle control via oral gavage. The body weight, viral load in the lungs, and pathological changes in the lung-intestine tissues were measured. Fecal samples were collected for 16S rRNA gene sequencing and non-targeted GC/LC-MS/MS metabolic profiling to determine the characteristics of the intestinal microbiota and metabolic profile.ResultsMK-2206 treatment significantly reduced the viral load in the lungs of infected mice and the damage to the lung-intestinal tissues. The analysis of the intestinal microbiota showed that MK-2206 treatment restored the levels of the Firmicutes and Actinobacteria phyla, increased the abundance of probiotic bacteria such as Lactobacillus, and decreased the abundance of Acinetobacter and Desulfobacter. Metabolomics analysis revealed an increase in the abundance of succinic acid, and the combination of succinic acid and MK-2206 exhibited a stronger antiviral effect.ConclusionBy integrating multi-omics methods, we discovered that succinic acid can enhance the antiviral efficacy of MK-2206, and clarified the related interactions between the intestinal microbiota and metabolites, revealing the crucial role of the intestinal microenvironment in the host’s response to MK-2206 treatment for coronavirus infection.
Abstract from DOAJ. Public domain (CC0 1.0).
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