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. 2020 Sep 7;9(9):2042. doi: 10.3390/cells9092042

Figure 1.

Figure 1

Virus-inflicted membrane damage. After binding to cell-surface receptors, viruses are internalized through endocytosis. Once in the endosome, adenovirus capsid undergoes partial disassembly and releases protein VI. The increase of ceramide concentration enhances the binding of protein VI to the endosomal membrane and its subsequent rupture. Polyomavirus-containing endosomes are targeted to the endoplasmic reticulum (ER) where the virus undergoes conformational changes to penetrate the ER-membrane and escape to the cytosol. Parvovirus and reovirus require a pH drop and the action of endosomal cathepsins to induce conformational rearrangements, disrupt the endosome, and reach the cytosol. After endocytosis and conformational changes, picornaviruses rely on a cellular lipid-modifying enzyme (PLA2G16) to facilitate the translocation of its genome via selective pores across the endosomal membrane. See Section 1 for further details. Abbreviations: ER, endoplasmic reticulum; Hsc70, Heat shock cognate 71 kDa protein; Hsp105, Heat shock protein 105 kDa; PLA2G16, phospholipase A2 group XVI.