Figure 1. The generalised overview of OV-induced anti-tumour immunity. Initially, OVs infect primary cancer cells and cause direct oncolysis via inducing autophagy, increasing proteasome activity, and upregulating ROS caused by ER stress and genotoxic stress upon the infection. Subsequently, DAMPs and PAMPs trigger TLR, a major sub-family of the PRRs, and activate APCs. APC/DC uptake TAAs/TANs and express them to immune cells such as CD8+ T cells and CD4+ T cells through MHC I - TCR and MHC II - TCR interactions, respectively. The releasing cytokines and chemokines recruit both innate immune cells such as neutrophils, macrophages, NK cells, and DC, and adaptive immune cells such as T cells and B cells to the infected sites. In addition, APC helps stimulating and manipulating CD8+ T cells and NK cells to release granzymes and perforin causing apoptosis of cancer cells. Furthermore, cytotoxic T lymphocytes can migrate to a distant tumour, recognize tumour antigens, and kill cancer cells.9, 14, 46, 48, 59, 60 APC: antigen presenting cells; ATP: Adenosine triphosphate; DAMPs: damage-associated molecular patterns; DC: dendritic cells; ER: endoplasmic reticulum; GM-CSF: granulocyte macrophage colony-stimulating factor; HSP: heat shock protein; HMGB1: high mobility group protein; MHC: major histocompatibility complex; NK cell: natural killer cell; OV: oncolytic virus; PAMPs: pathogen-associated molecular patterns; PRR: pattern recognition receptor; ROS: reactive oxygen species; TAAs: tumour-associated antigens; TANs: tumour-associated neoantigens; TCR: T cell receptor; TLR: Toll-like receptor; TNF-α: tumour necrosis factor-α. Adapted from Kaufman et al.14

Figure 2. The design of a high potential therapeutic polymer-coated oncolytic viruses (PC-OVs) delivery system which is coated by electrostatic polygalactosyl-b-agmatyl (Gal32-b-Agm29) diblock copolymer with asialoglycoprotein receptor (ASGPR) for diagnosis of hepatocellular carcinoma in human hepatoma cell line HepG2 as a model. ****P < 0.0001. Reprinted from Garofalo et al.113 OV: oncolytic virus; PC: polymer-coated.

Figure 3. Schematic illustration of the fabrication of a liposome-encapsulated M1 virus platform (M-LPO) for tumour therapy in LoVo and Hep 3B cell lines. Reprinted with permission from Wang et al.120 Copyright 2019 American Chemical Society.

Figure 4. (A) The synthesis of adenovirus encapsulating cationic 1,2-dioleoyl-3-trimethylammonium-propane (DOTAP)-folate liposomes (Ad-Df). (B) The cellular penetration approaches of Ad-Df viral platform in various coxsackievirus and adenovirus receptor (CAR)-deficient cell lines. (C) Ad-Df is capable of entering the cells via endocytosis during no expression of CAR of the target cells, leading to transfect CAR-positive and -negative cells. (D) The cellular uptake into FR-positive cells can be enhanced by Ad-Df containing folate-conjugated lipid through FR-mediated endocytosis. Reprinted with permission from Huang et al.122 Copyright 2022 American Chemical Society. FR: Folate receptor; PEG(2000)-PE: 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(poly-ethylene glycol)-2000].

Figure 5. A hyaluronic acid-based nanohydrogel formulation for oncolytic viral delivery for anti-cancer therapy. Reprinted from Deng et al.127

Figure 6. Application of myxoma virus-loaded mesenchymal stem cells (MSCs) for pulmonary melanoma treatment. Reprinted from Hadry? et al.128

Figure 7. (A) Illustration of the preparation and in vivo experimental processes of cryo-shocked cancer cells as oncolytic adenovirus reservoir (OARs) for glioblastoma immunotherapy in a mouse glioblastoma model. (B) The administration mechanism of OARs via intratumoural injection. Reprinted with permission from Liu et al.135 Copyright 2022 American Chemical Society. DC: dendritic cell; OA: oncolytic adenovirus.