Abstract
Oncolytic viruses replicate and spread in tumors at the same time, resulting in increased cytotoxicity and the reversal of tumor immune suppression. Among other viruses, recombinant adenoviruses replicated in tumor cells were clinically tested via intratumoral or systemic administration. Although oncolytic virus replication kills tumor cells on its own, it may also activate the immune system, which can aid in tumor control. Viruses can be modified to improve their selectivity and effectiveness. Adenovirus genomes can be easily designed to incorporate various tumor-targeting pathways and therapeutic transgenes to improve antitumor properties. Poor tumor targeting, intratumoral expansion, and virocentric immune responses are all linked to low efficacy. As a result, more effective oncolytic adenoviruses that can be used alone or in combination with chemotherapy or immunotherapy are needed. Oncolytic Adenovirus (OAds) has long been considered a potential biotherapeutic agent against various cancers due to its ability to replicate cancer cells while remaining dormant in healthy cells selectively. In recent years, several preclinical studies using genetic engineering technology have increased antitumor OAds in various cancers. Systemic OAds administration is hampered by poor targeting tropism to healthy tissues, low-level ad receptors on tumor cells, and pre-existing neutralizing antibodies. Various discoveries have been made to overcome these barriers, including stem cells, nanoparticles, polymer shielding, extracellular vesicles, hydrogels, and microparticles (MPs). These carriers may improve Oncolytic viruses’ therapeutic efficacy by improving transfection, circulatory survival, cellular interactions, specific targeting, and immune response. The structure and biology of adenoviruses, the different types of OAds, and the efficacy of different carriers in the systemic administration of OAds were all examined in this review.
Keywords: Adenovirus, heparan sulfate proteoglycans (HSPGs), oncolytic Adenovirus (OAds), microparticles (MPs), CD46, conserved region (CR2)
Graphical Abstract
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