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The Respiratory syncytial virus fusion protein (F protein) is a class I viral fusion protein that mediates the merger of viral and cellular membranes, enabling viral entry into host cells. The RSV nucleoprotein (N protein) forms the structural core of the ribonucleoprotein complex by encapsidating the viral genome, protecting RNA from degradation, and serving as a template for RNA synthesis. The RSV M2-1 protein is a transcription antiterminator and processivity cofactor for the viral RNA-dependent RNA polymerase, enabling synthesis of full-length mRNA transcripts and interacting with both viral and host RNAs. All three proteins are essential for RSV replication, play unique roles in the viral life cycle, and are considered validated or investigational therapeutic targets, primarily for the prevention or treatment of RSV infection.
Inhibition of F protein prevents viral entry into host cells by blocking fusion; inhibition of M2-1 protein disrupts viral transcription, blocking production of viral mRNAs; inhibition of N protein would disrupt viral RNA encapsidation and replication.
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