Lost in translation: interferon-stimulated genes targeting flavivirus protein synthesis - PubMed
4 hours ago
- #Flavivirus
- #Translation control
- #Interferon-stimulated genes
- Flaviviruses depend on host translation machinery for protein synthesis, presenting a vulnerability targeted by interferon-stimulated genes (ISGs).
- ISGs employ diverse mechanisms: PKR and IFIT inhibit translation initiation by affecting initiation factors or cap recognition, while SLFN11 and SAMD9L disrupt elongation via codon- and tRNA-dependent processes.
- Additional ISGs like ZAP, SHFL, and ISG20 restrict translation by excluding viral RNAs from ribosomes or degrading them, highlighting selectivity based on features such as cap structure, nucleotide composition, codon usage, and RNA folding.
- Translation serves as a key host-virus conflict interface, allowing ISGs to achieve potent antiviral effects while sparing host protein synthesis by exploiting differences between viral and cellular mRNAs.
- This minireview integrates recent advances in ISGs targeting flavivirus protein synthesis into a unified framework, emphasizing translation as a promising target for selective antiviral strategies and innate immunity control.