Fast-Acting Virus Targets Most Melanoma Tumors

The green color shows where the vesicular stomatitis virus has infected rust-colored melanoma tumor cells after injection of the virus into the blood stream. The surrounding non-cancerous tissue is free of virus. Credit: Yale University

In a newly published study, Yale University researchers show that a fast-acting virus targets most melanoma tumors after injection into the blood stream of mice.

Yale researchers eradicated most melanoma tumors by exposing them to a fast-acting virus, they report in the June 15 edition of the Journal of Virology.

Melanoma is the deadliest type of skin cancer and can spread throughout the body and even into the brain.

“After injection into the blood stream of mice, the virus finds melanoma on its own, and is fast and aggressive with tumors,” said Anthony N. van den Pol, professor of neurosurgery at Yale School of Medicine, investigator for the Yale Cancer Center and senior author of the study. “Because the virus replicates rapidly, it can kill the melanoma before the immune system responds and kills the virus.”

In the process of eliminating the virus, the immune system may also begin to target and kill tumor cells, he added.

The researchers used the vesicular stomatitis virus — part of a family of viruses that include rabies and may generate flu-like symptoms in humans. The fast-acting virus ignored healthy melanocytes (the cells from which melanoma arises) but zeroed in on 19 melanoma tumors studied. In 70 percent of tumors tested, melanoma was eradicated completely, while the rest showed a more limited response to the virus.

If safety of the virus can be substantiated, the next target would be to begin trials in humans, van den Pol said.

Other Yale authors include Guido Wollmann, John N. Davis, and Marcus W. Bosenberg.

The study was funded by the National Institutes of Health.

Reference: “Highly Attenuated Recombinant Vesicular Stomatitis Virus VSV-12′GFP Displays Immunogenic and Oncolytic Activity” by Anthony N. van den Pol and John N. Davis, 15 January 2013, Journal of Virology.
DOI: 10.1128/JVI.01106-12