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• W2999300004 abstract "Oncolytic viruses (OVs) constitute a new and promising immunotherapeutic approach toward cancer treatment. This therapy takes advantage of the natural propensity of most tumor cells to be infected by specific OVs. Besides the direct killing potential (oncolysis), what makes OV administration attractive for the present cancer immunotherapeutic scenario is the capacity to induce two new overlapping, but distinct, immunities: anti-tumoral and anti-viral. OV infection and oncolysis naturally elicit both innate and adaptive immune responses (required for long-term anti-tumoral immunity); at the same time, the viral infection prompts an anti-viral response. In this review, we discuss the dynamic interaction between OVs and the triggered responses of the immune system. The anti-OV immunological events that lead to viral clearance and the strategies to deal with such potential loss of the therapeutic virus are discussed. Additionally, we review the immune stimulatory actions induced by OVs through different inherent strategies, such as modulation of the tumor microenvironment, the role of immunogenic cell death, and the consequences of genetically modifying OVs by arming them with therapeutic transgenes. An understanding of the balance between the OV-induced anti-tumoral versus anti-viral immunities will provide insight when choosing the appropriate virotherapy for any specific cancer. Oncolytic viruses (OVs) constitute a new and promising immunotherapeutic approach toward cancer treatment. This therapy takes advantage of the natural propensity of most tumor cells to be infected by specific OVs. Besides the direct killing potential (oncolysis), what makes OV administration attractive for the present cancer immunotherapeutic scenario is the capacity to induce two new overlapping, but distinct, immunities: anti-tumoral and anti-viral. OV infection and oncolysis naturally elicit both innate and adaptive immune responses (required for long-term anti-tumoral immunity); at the same time, the viral infection prompts an anti-viral response. In this review, we discuss the dynamic interaction between OVs and the triggered responses of the immune system. The anti-OV immunological events that lead to viral clearance and the strategies to deal with such potential loss of the therapeutic virus are discussed. Additionally, we review the immune stimulatory actions induced by OVs through different inherent strategies, such as modulation of the tumor microenvironment, the role of immunogenic cell death, and the consequences of genetically modifying OVs by arming them with therapeutic transgenes. An understanding of the balance between the OV-induced anti-tumoral versus anti-viral immunities will provide insight when choosing the appropriate virotherapy for any specific cancer. During the oncogenic process, cancer cells undergo multiple genetic and physiological changes that make them distinguishable from normal cells. Among these cancer-inherent hallmarks, tumor cells evolve to evade immune-mediated recognition and destruction, including the acquisition of defects in cellular anti-viral pathways, such as those mediated by the interferons (IFNs).1Hanahan D. Weinberg R.A. Hallmarks of cancer: the next generation.Cell. 2011; 144: 646-674Abstract Full Text Full Text PDF PubMed Scopus (34874) Google Scholar, 2Choi A.H. O’Leary M.P. Fong Y. Chen N.G. From benchtop to bedside: a review of oncolytic virotherapy.Biomedicines. 2016; 4: E18Crossref PubMed Scopus (30) Google Scholar, 3Filley A.C. Dey M. Immune system, friend or foe of oncolytic virotherapy?.Front. Oncol. 2017; 7: 106Crossref PubMed Scopus (52) Google Scholar Theoretically, every type of malignant cell is more susceptible to infection by at least some viruses, and therefore this natural propensity has been explored as an emerging anti-cancer therapy by the exploitation of oncolytic viruses (OVs) to selectively infect and kill cancer cells, while exerting minimal or no pathogenicity against the host.4Marelli G. Howells A. Lemoine N.R. Wang Y. Oncolytic viral therapy and the immune system: a double-edged sword against cancer.Front. Immunol. 2018; 9: 866Crossref PubMed Scopus (96) Google Scholar OVs either occur naturally and are exploited as genetically unmodified isolates (e.g., reovirus), which include wild-type and naturally attenuated strains, or they are genetically engineered (e.g., herpes simplex virus-1 [HSV-1], adenoviruses, vesicular stomatitis virus [VSV], measles virus [MV], vaccinia virus [VV], or myxoma virus [MYXV]), encompassing genetic edits to the virus genome to weaken viral pathogenicity, improve immunogenicity, and/or insert therapeutic genes (transgenes).5Coffey M.C. Strong J.E. Forsyth P.A. Lee P.W. Reovirus therapy of tumors with activated Ras pathway.Science. 1998; 282: 1332-1334Crossref PubMed Google Scholar, 6Strong J.E. Coffey M.C. Tang D. Sabinin P. Lee P.W. The molecular basis of viral oncolysis: usurpation of the Ras signaling pathway by reovirus.EMBO J. 1998; 17: 3351-3362Crossref PubMed Scopus (428) Google Scholar, 7Bell J. McFadden G. Viruses for tumor therapy.Cell Host Microbe. 2014; 15: 260-265Abstract Full Text Full Text PDF PubMed Google Scholar, 8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar, 9Bai Y. Hui P. Du X. Su X. Updates to the antitumor mechanism of oncolytic virus.Thorac. Cancer. 2019; 10: 1031-1035Crossref PubMed Scopus (0) Google Scholar, 10Torres-Domínguez L.E. McFadden G. Poxvirus oncolytic virotherapy.Expert Opin. Biol. Ther. 2019; 19: 561-573Crossref PubMed Scopus (16) Google Scholar When selecting for the appropriate OV treatment strategy, intrinsic characteristics should be taken into consideration. Each OV family will exhibit unique genome complexities, replication mechanisms, lytic properties, packaging capacities for transgenes, and immune response triggering capabilities to stimulate anti-tumoral immunity. Since different OVs will exhibit distinct tumor tropisms, it has been difficult to identify individual molecular biomarkers that predict specific anti-tumor efficacies for any OV.7Bell J. McFadden G. Viruses for tumor therapy.Cell Host Microbe. 2014; 15: 260-265Abstract Full Text Full Text PDF PubMed Google Scholar,11Harrington K. Freeman D.J. Kelly B. Harper J. Soria J.C. Optimizing oncolytic virotherapy in cancer treatment.Nat. Rev. Drug Discov. 2019; 18: 689-706Crossref PubMed Scopus (114) Google Scholar Concurrent with the properties of OVs, the tumor biology and immune landscape will also contribute to the outcome of the therapeutic approach. The tumor microenvironment (TME) typically exhibits an immunosuppressive milieu leading to the active subversion of effective anti-tumoral immunity. Tumors generally secrete soluble immunosuppressive mediators, including nitric oxide, and cytokines such as interleukin (IL)-10 and transforming growth factor-β (TGF-β).3Filley A.C. Dey M. Immune system, friend or foe of oncolytic virotherapy?.Front. Oncol. 2017; 7: 106Crossref PubMed Scopus (52) Google Scholar,8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar,12Prestwich R.J. Harrington K.J. Pandha H.S. Vile R.G. Melcher A.A. Errington F. Oncolytic viruses: a novel form of immunotherapy.Expert Rev. Anticancer Ther. 2008; 8: 1581-1588Crossref PubMed Scopus (128) Google Scholar In addition, regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) are recruited to the TME where they co-opt the capacity of the elements of the acquired immune response pathway to recognize and clear the tumor cells.8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar,11Harrington K. Freeman D.J. Kelly B. Harper J. Soria J.C. Optimizing oncolytic virotherapy in cancer treatment.Nat. Rev. Drug Discov. 2019; 18: 689-706Crossref PubMed Scopus (114) Google Scholar,12Prestwich R.J. Harrington K.J. Pandha H.S. Vile R.G. Melcher A.A. Errington F. Oncolytic viruses: a novel form of immunotherapy.Expert Rev. Anticancer Ther. 2008; 8: 1581-1588Crossref PubMed Scopus (128) Google Scholar The multiple and complementary mechanisms of action of OVs will be successful only if they ultimately reverse the local immunosuppression within the TME and create a sufficient pro-inflammatory and pro-immune environment within the tumor bed to re-establish acquired anti-tumoral responses to the resident cancer cells. Besides the recognized anti-tumor qualities of OVs, as a result of their ability to create a favorable microenvironment for the action of the immune system against unique cancer cell determinants, the anti-viral immunity triggered against viral antigens from the resultant infection is also a key player during OV-based therapies. Indeed, induced anti-viral immunity was once considered detrimental for OVs, since the activation of the immune system against the virus itself is expected to restrict the viral replication and spread, leading to a decrease in therapeutic efficacy. However, it has now been recognized that there are undeniably beneficial aspects on the OV infection being detected by the immune system.8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Following administration, the OV will infect tumor cells and hijack the cell’s protein synthesis, promoting the production of viral macromolecules, but it will also trigger the expression and recognition of “danger signals.” These are a consequence of a cascade of signaling events that culminate with the release of cytokines and damage-associated molecular patterns (DAMPs).4Marelli G. Howells A. Lemoine N.R. Wang Y. Oncolytic viral therapy and the immune system: a double-edged sword against cancer.Front. Immunol. 2018; 9: 866Crossref PubMed Scopus (96) Google Scholar,8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar,9Bai Y. Hui P. Du X. Su X. Updates to the antitumor mechanism of oncolytic virus.Thorac. Cancer. 2019; 10: 1031-1035Crossref PubMed Scopus (0) Google Scholar Additionally, OVs cause cancer cell killing by promoting cell lysis, a process known as oncolysis, followed by the release of infectious viral progeny that spread to surrounding tumor cells (amplification of oncolysis) as well as subproducts, including viral particles, pathogen-associated molecular patterns (PAMPs), DAMPs, tumor cell debris, and tumor-associated antigens (TAAs).3Filley A.C. Dey M. Immune system, friend or foe of oncolytic virotherapy?.Front. Oncol. 2017; 7: 106Crossref PubMed Scopus (52) Google Scholar,4Marelli G. Howells A. Lemoine N.R. Wang Y. Oncolytic viral therapy and the immune system: a double-edged sword against cancer.Front. Immunol. 2018; 9: 866Crossref PubMed Scopus (96) Google Scholar,8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar,13Davola M.E. Mossman K.L. Oncolytic viruses: how “lytic” must they be for therapeutic efficacy?.OncoImmunology. 2019; 8: e1581528Crossref PubMed Scopus (41) Google Scholar All of these processes contribute to the stimulation of the innate and adaptive anti-cancer immune responses locally and systemically. Besides oncolysis and anti-tumoral immunity, some OVs have been shown to have potent anti-angiogenic effects by triggering an acute disruption of the tumor vasculature.14Angarita F.A. Acuna S.A. Ottolino-Perry K. Zerhouni S. McCart J.A. Mounting a strategic offense: fighting tumor vasculature with oncolytic viruses.Trends Mol. Med. 2013; 19: 378-392Abstract Full Text Full Text PDF PubMed Scopus (25) Google Scholar, 15Breitbach C.J. Arulanandam R. De Silva N. Thorne S.H. Patt R. Daneshmand M. Moon A. Ilkow C. Burke J. Hwang T.H. et al.Oncolytic vaccinia virus disrupts tumor-associated vasculature in humans.Cancer Res. 2013; 73: 1265-1275Crossref PubMed Scopus (136) Google Scholar, 16Toro Bejarano M. Merchan J.R. Targeting tumor vasculature through oncolytic virotherapy: recent advances.Oncolytic Virother. 2015; 4: 169-181PubMed Google Scholar Indeed, successful oncolytic virotherapy relies on a balance between anti-viral pathways that eliminate the virus and pro-immune pathways that recognize cellular epitopes, TAAs, and neoantigens from the virus-infected tumor cells. Here, we discuss the dynamics between OV monotherapies and the immune system from two contrasting perspectives, as the immune system has a recognized and obligatory role in the outcome of virotherapies. On the one hand, we look at the different challenges that the immune system poses to restrict and impede OVs. On the other hand, we review the anti-cancer immunotherapeutic potential of OVs, particularly for immune barren tumors that are nonresponsive to immune checkpoint inhibitor (ICI) therapies, resulting from their ability to stimulate the anti-tumoral immunity in novel ways. The different therapeutic combinations involving OVs and ICIs are highly relevant for the field and are furthest advanced in the clinic, and the reader is referred to other reviews on this aspect of combinatorial virotherapy.17Chen C.Y. Hutzen B. Wedekind M.F. Cripe T.P. Oncolytic virus and PD-1/PD-L1 blockade combination therapy.Oncolytic Virother. 2018; 7: 65-77Crossref PubMed Google Scholar, 18LaRocca C.J. Warner S.G. Oncolytic viruses and checkpoint inhibitors: combination therapy in clinical trials.Clin. Transl. Med. 2018; 7: 35Crossref PubMed Google Scholar, 19Martin N.T. Bell J.C. Oncolytic virus combination therapy: killing one bird with two stones.Mol. Ther. 2018; 26: 1414-1422Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar, 20Russell L. Peng K.W. Russell S.J. Diaz R.M. Oncolytic viruses: priming time for cancer immunotherapy.BioDrugs. 2019; 33: 485-501Crossref PubMed Scopus (40) Google Scholar OV infection of cancer cells changes how antigens are presented to the immune system and is the key reason why novel anti-tumoral immunity is elicited. The cell-intrinsic aberrations of OV-infected cancer cells are linked to how they are perceived by the elements of the innate and acquired immune systems. However, following the virus colonization of the tumor, the host anti-viral immunity will become activated and mobilized to restrict virus replication and spread, culminating in viral clearance and elimination of the therapeutic effect.8Gujar S. Pol J.G. Kim Y. Lee P.W. Kroemer G. Antitumor benefits of antiviral immunity: an underappreciated aspect of oncolytic virotherapies.Trends Immunol. 2018; 39: 209-221Abstract Full Text Full Text PDF PubMed Scopus (71) Google Scholar Thus, the effective “time window” for most OVs to activate anti-tumoral immunity is generally within the first 1–2 weeks of administration, before the virus is cleared. One of the major challenges of OV immunotherapy is therefore to achieve a balance between the desirable triggering of new anti-tumoral immunity and the competing anti-viral immunity, while keeping undesired anti-viral effector processes from becoming the dominant response pathway that overwhelms the acquisition of acquired anti-tumoral immunity. Stated simply, how can one maximize the generation of immune responses directed against tumor antigens revealed from OV-infected cancer cells while minimizing the consequences of anti-viral responses against viral antigens? For some disseminated cancers and/or micrometastatic lesions that are not readily amenable to intratumoral injection, the delivery of OVs should be systemic (e.g., intravenous infusion), which represents a major technical challenge for OV treatment efficacy.21Ferguson M.S. Lemoine N.R. Wang Y. Systemic delivery of oncolytic viruses: hopes and hurdles.Adv. Virol. 2012; 2012: 805629Crossref PubMed Scopus (104) Google Scholar Besides the existence of a variety of physical barriers within the circulatory system, a potential obstacle is the presence of anti-viral antibodies that either pre-exist (e.g., patients that have been previously vaccinated with a related virus) or arise from treatment-induced neutralizing anti-viral antibodies (nAbs), since these both reduce the effective virus titer, hinder any repetitive OV systemic delivery regimen, and contribute to patient anti-viral immunity.11Harrington K. Freeman D.J. Kelly B. Harper J. Soria J.C. Optimizing oncolytic virotherapy in cancer treatment.Nat. Rev. Drug Discov. 2019; 18: 689-706Crossref PubMed Scopus (114) Google Scholar,22Niemann J. Woller N. Brooks J. Fleischmann-Mundt B. Martin N.T. Kloos A. Knocke S. Ernst A.M. Manns M.P. Kubicka S. et al.Molecular retargeting of antibodies converts immune defense against oncolytic viruses into cancer immunotherapy.Nat. Commun. 2019; 10: 3236Crossref PubMed Scopus (1) Google Scholar Methods involving masking viral surface proteins with polymeric materials have been developed to enhance protection against nAbs and extend viral circulation half-life.23O’Riordan C.R. Lachapelle A. Delgado C. Parkes V. Wadsworth S.C. Smith A.E. Francis G.E. PEGylation of adenovirus with retention of infectivity and protection from neutralizing antibody in vitro and in vivo.Hum. Gene Ther. 1999; 10: 1349-1358Crossref PubMed Scopus (0) Google Scholar, 24Fisher K.D. Stallwood Y. Green N.K. Ulbrich K. Mautner V. Seymour L.W. Polymer-coated adenovirus permits efficient retargeting and evades neutralising antibodies.Gene Ther. 2001; 8: 341-348Crossref PubMed Scopus (281) Google Scholar, 25Zeng Q. Han J. Zhao D. Gong T. Zhang Z. Sun X. Protection of adenovirus from neutralizing antibody by cationic PEG derivative ionically linked to adenovirus.Int. J. Nanomedicine. 2012; 7: 985-997PubMed Google Scholar, 26Khalil I.R. Khechara M.P. Kurusamy S. Armesilla A.L. Gupta A. Mendrek B. Khalaf T. Scandola M. Focarete M.L. Kowalczuk M. Radecka I. Poly-gamma-glutamic acid (γ-PGA)-based encapsulation of adenovirus to evade neutralizing antibodies.Molecules. 2018; 23: E2565Crossref PubMed Scopus (4) Google Scholar Recently, Francini et al.27Francini N. Cochrane D. Illingworth S. Purdie L. Mantovani G. Fisher K. Seymour L.W. Spain S.G. Alexander C. Polyvalent diazonium polymers provide efficient protection of oncolytic adenovirus enadenotucirev from neutralizing antibodies while maintaining biological activity in vitro and in vivo.Bioconjug. Chem. 2019; 30: 1244-1257Crossref PubMed Scopus (3) Google Scholar developed a new class of polyvalent diazonium polymers to coat and shield the oncolytic adenovirus enadenotucirev, resulting in one of the first reports on complete ablation of nAb binding at polymer concentrations 10- to 20-fold lower than what was previously reported. Importantly, coating did not cause permanent inactivation of the OV. Also in the oncolytic adenovirus field, a recent strategy involved redirecting the viral nAbs against the tumor cell surface, showing how one of the limiting factors of using OVs would become reconfigured to become a beneficial feature of cancer immunotherapy.22Niemann J. Woller N. Brooks J. Fleischmann-Mundt B. Martin N.T. Kloos A. Knocke S. Ernst A.M. Manns M.P. Kubicka S. et al.Molecular retargeting of antibodies converts immune defense against oncolytic viruses into cancer immunotherapy.Nat. Commun. 2019; 10: 3236Crossref PubMed Scopus (1) Google Scholar This method comprises the use of a recombinant bifunctional adaptor protein with the ability of capturing adenoviral-specific nAbs but also recognizes tumor cells through a polysialic acid-specific single-chain variable fragment (scFv). To shield OVs from their own induced immunogenicity, which triggers the production of nAbs, encapsulation of the viral agent has been widely applied in the oncolytic adenovirus field. One of these cloaking methods consists of using specialized subcellular structures named extracellular vesicles (EVs) that originate from plasma membrane. Cancer cell-derived EVs transporting oncolytic adenovirus (Ad5D24) exhibited a tumor-selective delivery in a lung carcinoma model.28Garofalo M. Saari H. Somersalo P. Crescenti D. Kuryk L. Aksela L. Capasso C. Madetoja M. Koskinen K. Oksanen T. et al.Antitumor effect of oncolytic virus and paclitaxel encapsulated in extracellular vesicles for lung cancer treatment.J. Control. Release. 2018; 283: 223-234Crossref PubMed Scopus (12) Google Scholar,29Garofalo M. Villa A. Rizzi N. Kuryk L. Mazzaferro V. Ciana P. Systemic administration and targeted delivery of immunogenic oncolytic adenovirus encapsulated in extracellular vesicles for cancer therapies.Viruses. 2018; 10: E568Crossref PubMed Scopus (12) Google Scholar In addition, tumor cell-derived microparticles, a specific type of vesicle (0.1–1 μM), have proven also to be efficient carriers for oncolytic adenovirus.30Ran L. Tan X. Li Y. Zhang H. Ma R. Ji T. Dong W. Tong T. Liu Y. Chen D. et al.Delivery of oncolytic adenovirus into the nucleus of tumorigenic cells by tumor microparticles for virotherapy.Biomaterials. 2016; 89: 56-66Crossref PubMed Scopus (26) Google Scholar Alternatively to the encapsulation in fragments of the plasma membrane, the use of liposomes to wrap OVs has been widely applied to adenoviruses, and more recently to alphavirus M1.31Mendez N. Herrera V. Zhang L. Hedjran F. Feuer R. Blair S.L. Trogler W.C. Reid T.R. Kummel A.C. Encapsulation of adenovirus serotype 5 in anionic lecithin liposomes using a bead-based immunoprecipitation technique enhances transfection efficiency.Biomaterials. 2014; 35: 9554-9561Crossref PubMed Scopus (18) Google Scholar, 32Aoyama K. Kuroda S. Morihiro T. Kanaya N. Kubota T. Kakiuchi Y. Kikuchi S. Nishizaki M. Kagawa S. Tazawa H. Fujiwara T. Liposome-encapsulated plasmid DNA of telomerase-specific oncolytic adenovirus with stealth effect on the immune system.Sci. Rep. 2017; 7: 14177Crossref PubMed Scopus (4) Google Scholar, 33Wang Y. Huang H. Zou H. Tian X. Hu J. Qiu P. Hu H. Yan G. Liposome encapsulation of oncolytic virus M1 to reduce immunogenicity and immune clearance in vivo.Mol. Pharm. 2019; 16: 779-785Crossref PubMed Scopus (1) Google Scholar All of these are recent reports on different approaches on how oncolytic adenoviruses can ghost the immune system and get protection against nAbs. Nonetheless, it would be relevant to further investigate whether such concepts could be applied to other OVs. A related strategy applied to diverse OV platforms to counteract nAb inactivation consists of a cell-based carrier system, i.e., using different cell types as “shielding vehicles” pre-loaded ex vivo with OVs. These carrier cells are used as Trojan horses, hiding the OVs from recognition and attack by the immune system, which allows a longer therapeutic window, and they have shown the ability to traffic into tumor beds and release their viral cargo there.34Willmon C. Harrington K. Kottke T. Prestwich R. Melcher A. Vile R. Cell carriers for oncolytic viruses: Fed Ex for cancer therapy.Mol. Ther. 2009; 17: 1667-1676Abstract Full Text Full Text PDF PubMed Scopus (126) Google Scholar,35Ramírez M. García-Castro J. Melen G.J. González-Murillo Á. Franco-Luzón L. 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MSCs, for example, are considered attractive candidates for cancer therapy due to low immunogenicity, strong tumor-tropic homing properties, and lack of stimulation of sentinel lymphocyte" @default.
• W2999300004 created "2020-01-23" @default.
• W2999300004 creator A5033046282 @default.
• W2999300004 creator A5040591138 @default.
• W2999300004 creator A5046624504 @default.
• W2999300004 date "2020-06-01" @default.
• W2999300004 modified "2023-10-16" @default.
• W2999300004 title "Oncolytic Viruses and the Immune System: The Dynamic Duo" @default.
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