EIF3A and infection: Our RNAi experiments and functional assays support the following conclusions: 1) OCTR-1 inhibits expression of specific protein synthesis factors, such as ribosomal protein RPS-1 and translation initiation factor EIF-3.J, which reduces infection-triggered protein synthesis and UPR; 2) upregulation of UPR proteins and elevated UPR in octr-1(ok371) animals contribute to their enhanced immunity; 3) RPS-1 and EIF-3.J contribute to the elevated UPR in infected octr-1(ok371) animals; and 4) activation of the OCTR-controlled immune response is dependent on active translation.