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. 2021 Sep 25;9:71. doi: 10.1186/s40364-021-00318-4

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — Underlying mechanisms responsible for the antitumor effects of oncolytic viruses (OVs). (1) OVs can directly infect and lyse cancer cells. (2) OVs infect and lyse vascular endothelial cells, and recruit neutrophils, which promote coagulation and thrombosis to destroy blood vessels and inhibit angiogenesis. (3) OVs recruit dendritic cells (DCs), macrophages, neutrophils and T cells into the tumor microenvironment thus transforming “cold” tumors into “hot” tumors. (4) Lysed cancer cells release DAMPs/PAMPs/TAAs, which are recognized by DCs resulting in activation of CD4 + T and CD8 + T cells to kill cancer cells. (5) OVs can be armed with transgene target gene expression, which enhances the antitumor effect