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. 2021 Oct 29;11:687631. doi: 10.3389/fonc.2021.687631

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Copyright © 2021 Kitsou, Iliopoulou, Spoulou, Lagiou and Magiorkinis

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Oncogenic mechanisms in the development of MCPyV-related MCC: Indirect binding of p53 and inhibition of Rb proteins due to LT and tLT antigens of MCPyV lead to cellular immortalization and malignant transformation. LT and sT antigens contribute to the evasion of the immune system mechanisms by downregulating MHC-I and TLR-9. Viral DNA integration to the host genome participates in genome instability. (MCPyV, Merkel Cell Polyomavirus; MCC, Merkel Cell Carcinoma; LT, Large T; tLT, truncated Large T; sT, small T, MHC-I, Major Histocompatibility Complex Class I; TLR-9, Toll-like receptor 9; TCR, T-cell receptor). Created in BioRender.com.