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Hantaan virus (HTNV) infection can cause hemorrhagic fever with renal syndrome (HFRS) in humans, and currently, there are no long‐standing protective vaccines or specific antivirals available. Guanylate‐binding protein 1 (GBP1) is an interferon‐stimulated gene that defends against various pathogen infections. However, the function of GBP1 in HTNV infection remains unknown. Here, we describe how GBP1 prevents HTNV infection by obstructing virus entry. We found that HTNV infection induced GBP1 expression and that overexpression of GBP1 inhibited HTNV infection, while knockout of GBP1 had the opposite effect. Interestingly, GBP1 did not affect interferon (IFN) signaling during HTNV infection. Instead, GBP1 prevented HTNV from entering cells through clathrin‐mediated endocytosis (CME). We also discovered that GBP1 specifically interacted with actin but not dynamin 2 (DNM2) and made it difficult for DNM2 to be recruited by actin, which may account for the suppression of CME during HTNV infection. These findings establish an antiviral role for GBP1 in inhibiting HTNV infection and help us better understand how GBP1 regulates HTNV entry and could potentially aid in developing treatments for this virus. [ABSTRACT FROM AUTHOR]

It is becoming increasingly clear that maintaining the equilibrium of gut microbiota homeostasis during viral infections, such as Hantaan virus (HTNV), is of paramount importance. In order to gain insight into the role of NOD-like receptors in the immune system, we conducted a comparative study between C57BL/6 and Nlrx1-/- mouse models to analyze changes in the gut microbiota after HTNV infection. Our findings revealed an increase in the ratio of Firmicutes to Bacteroides in Nlrx1-/- mice, suggesting a potential link to inflammation. In addition, a comprehensive analysis of serum metabolomics revealed that differential metabolites were mainly concentrated in amino acid metabolism and lipid metabolism. Amino acid metabolism mainly involves arginine, lysine, and histidine metabolism, while lipid metabolism is mainly related to glycerophospholipid metabolism and fatty acid synthesis. Analysis of the correlation between microbiota and metabolites revealed an inverse relationship between Bacteroidetes and metabolites related to glutamine metabolism, while Firmicutes were directly associated with these metabolites. Furthermore, we observed a negative correlation between the presence of Actinobacteria, Proteobacteria, and Patescibacteria and the metabolites related to polyunsaturated fatty acids (PUFAs). Our results demonstrate that HTNV infection causes changes in the composition of gut microbiota in both Nlrx1-/- and wild-type (WT) mice. Moreover, the fecal microbiota and serum metabolites of Nlrx1-/- mice display notable differences at various developmental stages. Investigating this further may help to improve our understanding of the pathogenesis of HTNV and provide potential therapeutic options. [ABSTRACT FROM AUTHOR]