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. 2020 Nov 10;19:158. doi: 10.1186/s12943-020-01275-6

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© The Author(s) 2020

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 — Limiting factors affecting the therapeutic effects of oncolytic virotherapy. Viral infection induces the generation of type 1 IFNs by PRR-mediated innate immunity. At the same time, tumor cells may shift sensitivity from the permissive status to a resistant status following durable virotherapy. The dense network of the extracellular matrix also hinders viral spread in tumors. Systemic delivery of naked therapeutic viruses may result in attenuation of viral activity and copies due to phagocytosis by the mononuclear phagocyte system and the neutralizing effects of serum antiviral factors. In addition, there is high interstitial fluid pressure in tumor tissues, which prevents effectively extravasation of the virus from the blood vessel