"We can see exactly how the virus breaks into the cancer cells, while leaving other cells untouched," Bostina explained.
The virus was a strong contender for effective virotherapy because it selectively targeted a receptor found only in tumour cells in more than 60 per cent of human cancers.
The receptor, a protein called ANTXR1, was expressed on tumours, but it had a cousin, ANTXR2, that only appeared on healthy tissues.
SVV didn't bind with the similar receptor on healthy cells, and only showed a strong affinity for ANTXR1.
SVV had already demonstrated its cancer-fighting abilities in clinical trials, but there was one problem – the body built up immunity to the virus within just a couple of weeks.
"This structure teaches us which part of the virus is essential for binding to the receptor and which is not," Bostina said.
"If we want to make the virus more efficient at invading cancer cells, we can leave intact the part that interacts with the cancer cells and modify the rest so the virus can escape the attack of the immune system."
Study lead author and Otago University PhD candidate Nadishka Jayawardena said he'd "always been intrigued" by how naturally occurring micro-organisms could be used for human benefit.
"Being able to work on a virus that can kill cancers is very rewarding, especially knowing that one day our findings could potentially lead to tackling a major global health issue."