Not only does the virus cause cancer cells to die, it also forces them to release proinflammatory chemokines and cytokines, which then causes the patient's immune system to fight the disease. New research has also revealed that reovirus infected cancer cells secrete proteins that, even when isolated, result in the death of cancer cells.

Normal human cells are protected from reovirus infection by a protein called PKR. However, a cellular signaling protein (Ras), which can block PKR activity, is abnormally triggered in many types of cancer, and it provides a window of opportunity for reovirus infection. A multicenter study, involving laboratories in the United Kingdom and the United States, gathered growth media from reovirus infected melanoma cells. The researchers showed that this media contained a range of small proinflammatory proteins, including an interleukin (IL-8) and type 1 interferon (INF-β), which recruited and activated white blood cells, specifically natural killer (NK) cells, dendritic cells (DCs), and antimelanoma cytotoxic T cells (CTLs).

While the precise details behind this mode of action of cell signaling in response to viral infection are unclear, the release of cytokines was dependent on both "inactive" PKR and a specific nuclear factor (NF-κβ). According to Prof. Alan Melcher, from the Leeds Institute of Molecular Medicine (UK), and one of the investigators of the study, "bystander immune-mediated therapy may well be an important component in the treatment of cancer by reoviruses, and may have potential in treating cancer even in the absence of live virus."

The study's findings were published February 20, 2011, by BioMed Central's open access journal Molecular Cancer.

Related Links:
Leeds Institute of Molecular Medicine