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Figure 1 | Veterinary Research

Figure 1

From: Membrane fusion, potential threats, and natural antiviral drugs of pseudorabies virus

Figure 1

PrV entry mechanism through membrane fusion. A PrV virion simulation diagram. PrV virions are composed of four structural elements: a lipidic envelope containing non-glycosylated trans-membrane proteins UL20, UL43, US9, and glycosylated membrane proteins gB, gC, gD, gE, gG, gH, gI, gK, gL, gM, and gN; a dense protein tegument layer, generally classified as outer and inner tegument proteins; an icosahedral protein capsid; and a linear double-stranded DNA genome. B The essential viral glycoproteins gD, gH/L, gB, and host receptor nectin-1 for the PrV entry mechanism. C The viral-cell membrane fusion process. Attachment: PrV binds with HS via its gC; this step enhances entry but is not required for fusion. Receptor binding and attachment stabilization: gD binds to its nectin-1 receptor to stabilize PrV binding; the C-terminus of the gD ectodomain exposes the receptor binding site, completing gD binding to nectin-1. This transmits a signal to activate gH/L, which may come directly from the C-terminus moving along the gD ectodomain or from other interaction sites exposed by the C-terminus moving and physical interaction between gD and gH/L. Triggering and gB rearrangement: gH/L transmits this signal via the physical binding of gH/L and gB ectodomain and the gH CTD interaction with the gB CTD to trigger core fusion protein gB. Upon triggering, the prefusion gB conformation undergoes rearrangement, emerging as a more stable post-fusion gB conformation. Fusion loop insertion: the fusion loops of post-fusion gB insert into the target cell membrane. Fusion: as gB shrinks, the fusion loops gradually drive the cell membrane closer to the gB TMD completing the viral-cell membrane fusion. Finally, the capsid associated with inner tegument proteins enter the target cell.

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