Years of research have allowed scientists at Purdue University to manipulate a viral vector, engineering a Sindbis virus to target and kill cancer cells, plus annihilate its native infection preferences, according to a press release.
“This virus had been known to be a good vector for delivering therapeutic cargo, however it naturally infected all kinds of cells, and these diversions would compete with what we were instructing it to target,” Richard Kuhn, the director of Purdue’s Bindley Biosciences Center, said in the release. “We have now overcome a major challenge by not only inserting a targeting molecule of our choice, but also successfully stripping the virus of its native entry preferences. This was a big step in unlocking the potential of developing this virus into a platform for both targeted drug delivery, where it would sneak drugs inside cancer cells, and oncolytic virotherapy, where the virus itself destroys cancer cells.”
The approach used applies methods that were once only used to manipulate proteins–including directed evolution, according to the abstract in the Journal of Virology. That strategy is called the tandem selection and enrichment system (TSES), which “expands the scope of directed evolution and can be easily extended to other targeting molecules and viral systems.”
When Investment Rhymes with Canada
Canada has a proud history of achievement in the areas of science and technology, and the field of biomanufacturing and life sciences is no exception.
“These experiments demonstrate that these two methods can be combined and used to create complex molecular machines, like this viral vector with a tailored targeting receptor,” Kuhn said in the release. “We’ve now reached the point where we can easily change the virus to carry a variety of cargos and to seek out specific types of cells. We know where and how to add the characteristics we want and eliminate those that we do not.”
From the press release:
Through standard rational design procedures the team inserted a human epidermal growth factor, or EGF, targeting sequence into the genome of the virus, and changed some of its amino acids to stabilize the addition, Kuhn said. . . . When the ESV1 virus binds to the EGF receptor on a cancer cell it triggers a natural signal for the cell to internalize, or consume, the growth factor and the virus is carried in along with it, he said.
“A healthy cell will easily be able to manage this virus, but cancer cells will gobble it up in overwhelming and deadly amounts. . . .”
The resulting virus, named Epidermal Growth Factor Receptor Specific Virus 1, or ESV1, doesn’t replicate well and its effects will be more like a drug than a viral infection within a patient. It will likely only remain in the body for a short period of time and will not continue to infect the body. Patients will likely need more than one dose over the course of a cancer therapy, he said.
For more on the science behind TSES and how the process works, click here.
Follow MedCity News on Facebook and Twitter for more updates.
