Maize chlorotic mottle virus (MCMV) interacts in mixed infections with potyviruses to cause maize lethal necrosis disease (MLND). In 2011 MLND appeared for the first time in East Africa and China. No resistance genes to MCMV are known, thus MLND remains a devastating disease in East Africa. Similar to other members of the Tombusviridae family, MCMV RNA lacks the 5’ cap required for translation of host mRNAs, and instead harbors a cap-independent translation element (CITE) in the 3’ untranslated region (UTR). Because this differs from host translation, here we characterized the MCMV translation mechanism as a potential target for engineered resistance. The MCMV 3’ CITE (MTE) both resembles and differs from the well-characterized panicum mosaic virus class of 3’ CITE (PTE). We used mutagenesis and chemical probing to show that, like the PTE, the MTE forms a branched stem-loop structure with a purine bulge containing a hypermodifiable G. Unlike PTEs, no pseudoknot involving the purine bulge was evident. Translation and infectivity assays showed that the MTE must base pair to the 5’ UTR to facilitate translation initiation and virus replication. Gel shift assays revealed that, like the PTE, the uncapped MTE binds cap-binding translation initiation factor eIF4E. Thus, eIF4E binds the MTE differently than host mRNAs which require a 5’ cap for eIF4E binding, and it should be possible to identify eIF4E mutants that bind only capped mRNA and not the MTE. Introducing such mutations into maize eIF4E genes may provide resistance to MCMV.