A modified oncolytic measles virus exhibits strong immunotherapeutic potential through RIG-I activation by defective viral genomes

A modified oncolytic measles virus exhibits strong immunotherapeutic potential through RIG-I activation by defective viral genomes | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Article A modified oncolytic measles virus exhibits strong immunotherapeutic potential through RIG-I activation by defective viral genomes Frederic Tangy, Aleksandr Barinov, Heidy Vera-Peralta, Joëlle Nader, and 21 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-7774994/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted You are reading this latest preprint version Abstract Live-attenuated measles virus (MV) infects cancer cells through the CD46 receptor, commonly overexpressed in tumors, and replicates preferentially in cells with impaired type I interferon (IFN-I) response. To enhance immune stimulation, we engineered a C protein–deficient MV (MVdeltaC), thus eliminating a key viral antagonist of innate immunity. MVdeltaC exhibited potent oncolytic activity in a broad panel of human tumor cell lines, with a vast majority of them showing high sensitivity. This enhanced efficacy is dependent on RIG-I stimulation, mainly through the generation of defective viral genomes, which trigger apoptosis, robust IFN-I signaling and massive CXCL10 production. MVdeltaC infection induced immunogenic cell death, the release of danger signals, and the maturation of dendritic cells. In vivo, MVdeltaC significantly reduced tumor burden in xenografts and patient-derived xenograft (PDX) models. Intratumoral MVdeltaC administration in immunocompetent A/J mice grafted with syngeneic neuroblastoma led to complete tumor rejection in 90% of animals and long-term antitumor memory. Efficacy was dependent on CD8+ T and NK cells and was further enhanced by anti- CTLA-4 treatment or CD4+ T cell depletion. Prior measles immunization accelerated tumor clearance, indicating memory-boosted antitumor responses. These findings support the clinical potential of MVdeltaC as a strong RIG-I activator for next-generation large-spectrum anticancer therapy. Health sciences/Oncology/Cancer/Cancer therapy/Cancer immunotherapy Biological sciences/Immunology/Immune cell death Biological sciences/Immunology/Innate immunity/Pattern recognition receptors/RIG-I-like receptors Health sciences/Oncology/Cancer/Mesothelioma Biological sciences/Cancer/Cancer therapy/Tumour vaccines Full Text Additional Declarations Yes there is potential Competing Interest. Five coauthors are employees of Oncovita (AB, FT, HVP, PNF, VR). FT and MG are cofounders of Oncovita. JFLB is chairman of Oncovita. FT, MG, JFF, CC are inventors of the US patent N° 10,314,905 B2 and the EU patent N° EP2 948 157B1 (USE OF A GENETICALLY MODIFIED INFECTIOUS MEASLES VIRUS WITH ENHANCED PRO-APOPTOTIC PROPERTIES (MV-DELTAC VIRUS) IN CANCER THERAPY) granted for the treatment of aggressive solid tumors. Supplementary Files Barinovelal2025Supplementaryfigures.pdf Supplementary figures Meso13MV.avi Infection of Meso 13 mesothelioma cells by MV Meso13MVdeltaC.avi Infection of Meso 13 mesothelioma cells by MVdeltaC Cite Share Download PDF Status: Under Review Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-7774994","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Article","associatedPublications":[],"authors":[{"id":539348100,"identity":"f1eb0c11-584b-48be-ad8b-81cc6ac6e73b","order_by":0,"name":"Frederic 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FT and MG are cofounders of Oncovita. JFLB is chairman of Oncovita. FT, MG, JFF, CC are inventors of the US patent N° 10,314,905 B2 and the EU patent N° EP2 948 157B1 (USE OF A GENETICALLY MODIFIED INFECTIOUS MEASLES VIRUS WITH ENHANCED PRO-APOPTOTIC PROPERTIES (MV-DELTAC VIRUS) IN CANCER THERAPY) granted for the treatment of aggressive solid tumors.","formattedTitle":"A modified oncolytic measles virus exhibits strong immunotherapeutic potential through RIG-I activation by defective viral genomes","fulltext":[],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":false,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":true,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":true,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"nature-portfolio","isNatureJournal":true,"hasQc":false,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"","title":"Nature Portfolio","twitterHandle":"","acdcEnabled":false,"dfaEnabled":false,"editorialSystem":"ejp","reportingPortfolio":"","inReviewEnabled":true,"inReviewRevisionsEnabled":false},"keywords":"","lastPublishedDoi":"10.21203/rs.3.rs-7774994/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-7774994/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eLive-attenuated measles virus (MV) infects cancer cells through the CD46 receptor, commonly overexpressed in tumors, and replicates preferentially in cells with impaired type I interferon (IFN-I) response. To enhance immune stimulation, we engineered a C protein–deficient MV (MVdeltaC), thus eliminating a key viral antagonist of innate immunity. MVdeltaC exhibited potent oncolytic activity in a broad panel of human tumor cell lines, with a vast majority of them showing high sensitivity. This enhanced efficacy is dependent on RIG-I stimulation, mainly through the generation of defective viral genomes, which trigger apoptosis, robust IFN-I signaling and massive CXCL10 production. MVdeltaC infection induced immunogenic cell death, the release of danger signals, and the maturation of dendritic cells. In vivo, MVdeltaC significantly reduced tumor burden in xenografts and patient-derived xenograft (PDX) models. Intratumoral MVdeltaC administration in immunocompetent A/J mice grafted with syngeneic neuroblastoma led to complete tumor rejection in 90% of animals and long-term antitumor memory. Efficacy was dependent on CD8+ T and NK cells and was further enhanced by anti- CTLA-4 treatment or CD4+ T cell depletion. Prior measles immunization accelerated tumor clearance, indicating memory-boosted antitumor responses. 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