Figure 1.

Schematic representation of genomic Merkel cell polyomavirus (MCPyV) insertion, T-antigen expression and induction of oncogenic alternative Δ exon 6–7 TrkAIII splicing in Merkel cell carcinoma (MCC), leading to spontaneous intracellular Δ exon 6–7 TrkAIII activation within endoplasmic reticulum intermediate and COP1 vesicle membrane compartments (ERGIC/COP1), inhibition of anterograde Δ exon 6–7 TrkAIII transport, retrograde-activated Δ exon 6–7 TrkAIII transport back to the endoplasmic reticulum (ER), centrosome and mitochondria, and oncogenic activity characterised by inositol-triphosphate 3-kinase (IP3K)/Akt survival signalling, centrosome amplification, an adaptive survival ER-stress response, enhanced resistance to oxidative stress and stress-induced aerobic glycolysis.