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Cancer-Killing Viruses Employ Multiple Mechanisms

e and adaptive immune responses, specifically communication between dendritic and natural killer cells (part of innate immunity) and certain types of T cells (from the adaptive immune system).

“We’ve understood the mechanism of action of reovirus replication in cancer for a number of years,” explains Dr. Matt Coffey, Chief Scientific Officer at Oncolytics, “but we also observed that often tumors continued to shrink after the virus was gone.” Immunologic work now suggests that reovirus exposure is “educating” the immune system to recognize and kill the same cancer cells that are attacked by reovirus. “If you can teach the immune system to recognize cancer cells, it may be possible to fight off the disease for much longer than we originally anticipated.”

Reovirus is an oncolytic virus that specifically targets tumor cells containing an active form of ras, a genetic mutation found in many types of cancer but not in normal cells. Because of the reovirus genetic makeup, it also appears to activate an immune response that spells double trouble for cancer cells.

Researchers hypothesized that reovirus activation of dendritic cells, which are key to early detection of infection (through the innate immune response), may “instruct” cells belonging to the adaptive immune response, namely natural killer cells and T cells, to attack the tumor even after the virus no longer remains in the body.

Experiments at respected institutions such as St. James University Hospital in Leeds and the Mayo Clinic in Rochester suggest that incubation of reovirus with human dendritic cells led to well-known signs of immune system activation. One of these is the release of cancer-fighting chemicals known as cytokines. Moreover, reovirus did not induce either productive infection (which generates many thousands of copies of the virus) or death in dendritic cells. In other words, although the dendritic cells were technically infected with reovirus, they
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