Oncolytic Viruses Expressing Cytokine IL-36γ for Cancer Therapy
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The targeted expression from a specific locus, such as the thymidine kinase gene, enables robust localized inhibitor production and a bystander effect through associated cell-penetrating peptides, thereby enhancing the overall STAT3 suppression in the tumor microenvironment. Unlike traditional therapeutic approaches, the virus’s selective replication and enhanced gene expression not only increase efficacy but also reduce off-target effects, offering a promising advancement in cancer treatment modalities. This technology stands out by integrating the targeted lytic action of an oncolytic virus with molecularly precise inhibition of a key cancer-promoting pathway.
The University of Pittsburgh researchers utilized these to deliver oncolytic virotherapy to cancer cells. Previous strategies have involved infection of cancer cells with HSV and replication of the virus leading to cell death (oncolytic viruses). However, poor replication efficiency of oncolytic viruses, along with “off-target” infection and associated side effects limits the use of this strategy.
This novel approach aims to remove residue 38 and use various single domain (VHH/SD) antibodies to target a tumor-specific epidermal growth factor receptor (EGFR) variant EGFRvIII to facilitate tumor cell infection. These novel oHSVs would be more selective to tumor cells allowing for more targeted treatment of cancer cells. In vitro testing in a U251 flank tumor model found these single-domain-based oHSVs could selectively infect tumor cells via EGFR dependent virus entry and demonstrated lateral spread compared to scFv-based oHSVs, while minimally infecting other cells.