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The Vesicular Stomatitis Virus (VSV) nucleocapsid protein (N) is a primary structural protein of the virus, belonging to the Rhabdoviridae family (UniProt P03521). Its main function is to coat the viral RNA genome, forming a ribonucleoprotein (RNP) complex that protects the RNA from degradation and serves as the template for the viral RNA-dependent RNA polymerase (Green et al., Science, 2006). The N protein must interact specifically with the viral phosphoprotein (P) to remain soluble and to facilitate the assembly of new nucleocapsids during viral replication (Leyrat et al., PLOS Pathogens, 2011). While VSV is a significant veterinary pathogen causing vesicular disease in livestock, it is also a prominent tool in biomedical research, serving as a platform for oncolytic virus therapy and vaccine vectors (NIH, 2023). Therapeutic strategies targeting the N protein focus on disrupting its ability to bind RNA or its essential interaction with the P protein, thereby halting the viral life cycle (Morin et al., Journal of Virology, 2013).
Inhibition of viral RNA encapsidation and disruption of the interaction between the nucleoprotein (N) and the phosphoprotein (P), which is essential for the viral polymerase complex activity (Morin et al., 2013).
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