Modified virus attacks cancer

BRITISH scientists have engineered a virus that would target and destroy cancer cells while leaving healthy tissue untouched.

Normal cells shut themselves down when they were infected with the virus, but the cancer cells did not. The Cancer Research UK team’s findings are reported in the journal Molecular Therapy.

Viruses infect the body by entering cells undetected and taking control of their machinery. Being able to enter a cell by stealth makes viruses a good tool to carry anti-cancer treatment directly into cancer cells.

The stumbling block is to ensure healthy cells are not damaged in the process.

Professor Nick Lemoine and colleagues at Bart’s and Queen Mary’s School of Medicine and Dentistry have created a modified virus that will do just that.

The anti-cancer virus lacks a gene viruses normally use to disguise themselves so they can sneak into the cell unnoticed.

Normal cells can recognise they are under attack by the modified virus and commit suicide to prevent it from replicating and infecting other cells.

But cancer cells are programmed differently and resist suicide at all costs.

This “selfishness” on the cancer’s behalf allows the engineered virus to replicate within the cancer cells and spread through the tumour.

When the team tested the virus in the laboratory, it thrived in the cancerous tissue but was eliminated from healthy tissue.

This should make it possible to create a highly selective anti-cancer treatment, say the researchers.

The next step is to put a toxic gene into the virus to poison the cancer cells.

The researchers believe only a small number of copies of the virus will be needed to be effective because the cancer makes more copies of the virus.

Professor Lemoine said: “The great thing about this strategy is that the cancer cell does all the hard work.”

This might make it possible to inject the modified virus into the patient’s bloodstream, unlike other viral therapies currently being developed that have to be injected directly into the tumour.