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Oncolytic viruses target and kill cancer cells without harming healthy cells by promoting an immune response against a tumor. However, they only work in a minority of patients. Findings from a new study identify potential mechanisms underlying the varied response to oncolytic virus therapies.
The authors of the cell study investigated the role of cancer-associated fibroblasts, a type of cell involved in the body’s immune and inflammatory responses. They infected cancer cells with herpes simplex virus, the only FDA-approved oncolytic virus, to determine how the fibroblasts mediate the tumor’s response to the virus.
They found that when fibroblasts come in contact with cancer cells, they activate pathways that mediate the expression of proinflammatory cytokines such as interferon beta-1. Interferons are proteins produced by the body’s cells as a defensive response to viruses. The ensuing inflammation prevents the virus from invading and replicating in the cancer cell, undermining the pathogen’s efficacy.
These findings identify potential mechanisms that mediate the body’s response to oncolytic viruses and suggest that targeting the pathways that mediate the expression of proinflammatory cytokines might be useful in future cancer therapies.
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