DDX3 Regulates the Cap-Independent Translation of the Japanese Encephalitis Virus via Its Interactions with PABP1 and the Untranslated Regions of the Viral Genome.

ABSTRACT: The translation of global cellular proteins is almost completely repressed in cells with flavivirus infection, while viral translation remains efficient. The mechanisms of flaviviruses evade host translational shutoff are largely unknown. Here, it is found that Japanese encephalitis virus (JEV) can adopt cap-independent (CI) translation to escape the host translational shutoff. Furthermore, the elements DB2 and sHP-SL within 3'UTR are involved in the regulation of CI translation, which is conserved in the genus Orthoflavivirus. By RNA affinity purification and mass spectrometry analysis, cellular DEAD-box protein 3 (DDX3) and poly(A)-binding protein 1 (PABP1) are identified as key factors in regulating CI translation of JEV via their interactions with DB2 and sHP-SL RNA structures. Mechani

SUBMITTER: Li C 

PROVIDER: S-EPMC12279179 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature