Figure 11

PCV2 virion trafficking in the endo-lysosomal network. The process of PCV2 infection begins with the virion attaching to GAGs or specific cell receptors. Viral particles gather on the surface of T-lymphoblasts. The signaling pathway of clathrin-mediated endocytosis is then activated, leading to the formation of clathrin-coated vesicles (CCVs). The vesicle delivers its viral content to the early endosome (EE), where sorting determines whether the vesicle is recycled to the cell surface. The EE containing the virus subsequently undergoes acidification and matures into the late endosome (LE). Virions transfer their genetic materials from the endosomal compartment to the cytoplasm through membrane permeabilization or lysis. Lysis typically occurs when the viral capsid induces a rupture in the endosomal membrane. This process is triggered by conformational changes in the capsid protein, resulting from binding to cell receptors, proteolysis, endosomal acidic pH, or changes in divalent cation concentrations. The outcome is either the release of the viral genome into the cytosol, especially when the endosome is very small and the expanding viral genome-ring destroys it or the residence of the viral genome in the endosome, especially when the endosome is big, and the viral genome cannot escape. The LE then fuses with the lysosome to form an endolysosome, within which the accompanying viral content is degraded until the remaining cargoes are either transported to lysosomes for final degradation or to other possible organelles. Relatively little is known about the other viral locations and the mechanistic interactions between PCV2 virions and the endo-lysosomal network. This figure is created with BioRender.