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Life cycle of the West Nile virus and key drug targets

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The West Nile virus initiates infection by binding to an as-yet unidentified receptor on the host cell surface. Entry into the host cell is mediated via clathrin-dependent endocytosis. Following internalization, the virus fuses with the vesicular membrane, releasing the gRNA into the cytoplasm. The gRNA is translated into a polyprotein precursor, which undergoes proteolytic cleavage to produce structural proteins (C, prM, E) and non-structural proteins (NS). The non-structural proteins form the replication complex, facilitating the synthesis of new gRNA. Structural proteins and replicated gRNA are assembled into nascent virions within the ER. The partially assembled virions are encapsidated and transported through the ERGIC to the Golgi apparatus. Final virion maturation occurs in the vesicles that are transported to the cell membrane, where furin cleaves prM to M, before the release of the newly formed infectious virus particles, which can now infect additional host cells. Several therapeutic targets have been identified along this pathway, such as the E protein, NS3 protease, NS5 RdRp, and the NS3-NS5 interaction interface. Abbreviations: C, Capsid protein; E, Envelope protein; ER, Endoplasmic Reticulum; ERGIC, ER-Golgi intermediate compartment; gRNA, genomic RNA; NS, Non-Structural protein; prM, pre-Membrane protein; RdRp, RNA-dependent RNA polymerase; WNV, West Nile Virus. Cropped from the original. (From: Kocabiyik DZ, Álvarez LF, Durigon EL, Wrenger C. West Nile virus - a re-emerging global threat: recent advances in vaccines and drug discovery. Front Cell Infect Microbiol 2025;15:1568031. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)