Promotes the GTP-dependent binding of aminoacyl-tRNA to the A-site of ribosomes during protein biosynthesis. Also plays a role in the regulation of autophagy and innate immunity. Recruits ATG5-ATG12 and NLRX1 at mitochondria and serves as a checkpoint of the RIG-I/DDX58-MAVS pathway. In turn, inhibits RLR-mediated type I interferon while promoting autophagy. Interacts with NLRX1 (PubMed:22749352). Interacts with ATG16L1 (PubMed:22749352). (Microbial infection) Interacts with human parainfluenza virus 3 matrix protein; this interaction inhibits RLR-mediated type I interferon production while promoting autophagy. (Microbial infection) Interacts with Hantaan hantavirus glycoprotein N; this interaction contributes to the virus-induced degradation of mitochondria by autophagy, which leads to degradation of MAVS and inhibition of type I interferon (IFN) responses. The disease is caused by variants affecting the gene represented in this entry. Belongs to the TRAFAC class translation factor GTPase superfamily. Classic translation factor GTPase family. EF-Tu/EF-1A subfamily.