Specifically, we confirmed that deletion of tbcm significantly increased the expression of genes related to mitochondrial dysfunction, such as TRIM39 and SARM1, until 4 h postinfection, which is a relatively early stage of infection, and suppressed the expression of SLC25A26, NDUFA8 and DTYMK, which are associated with maintaining mitochondrial homeostasis (Fig. 4C). This evidence concerns the gene SLC25A26 and infection.