TRIM7 inhibits encephalomyocarditis virus replication by activating interferon-? signaling pathway

Tripartite motif-containing protein 7 (TRIM7), the member of tripartite motif (TRIM) family, plays an important role in innate immune responses against viral infection. Among them, the function of TRIM7 in Encephalo-myocarditis virus (EMCV) infection has not been reported. Here, we found that TRIM7 inhibited the replication of EMCV through the type I interferon (IFN) signaling pathway. Interestingly, TRIM7 was down-regulated after EMCV infection in HEK293T cells. Further, overexpression of TRIM7 suppressed the replication of EMCV in HEK293T cells and enhanced the activity of IFN-I3 promoter. On the other hand, knockdown of the endogenous TRIM7 promoted EMCV infection and impaired the activity of IFN-I3 promoter. TRIM7 could regulate retinoic acid-inducible gene I (RIG-I)/ melanoma differentiation-associated gene 5 (MDA5)/ mitochondrial antiviral -signaling protein (MAVS) mediated IFN-I3 signaling pathway. Moreover, TRIM7 interacted with MAVS and they were co-located in HEK293T cells. We demonstrate that TRIM7 plays a positive role in IFN-I3 signaling pathway during EMCV infection and suppresses EMCV replication. Taken together, the presented results suggest that TRIM7 has a pivotal function in anti-EMCV infection, thereby providing a potential target for further development of anti-EMCV inhibitors.