Virus Seems Able to Destroy Latent HIV-Infected Cells

Jonathan Angel, MD, FRCPC, senior scientist and infectious disease physician at The Ottawa Hospital

Jonathan Angel, MD, FRCPC

Scientists say a viral therapy designed to target cancer cells seems capable of destroying HIV-infected cells, too.

Researchers in Canada have been experimenting with using the Maraba virus, known as MG1, to destroy cancer cells. The virus is able to attack cancer cells that are vulnerable because they have defective interferon signaling.

Jonathan Angel, MD, FRCPC, senior scientist and infectious disease physician at The Ottawa Hospital, said HIV-infected cells also have impaired interferon signaling. He therefore wondered if HIV cells would similarly be susceptible to a virus like MG1. He decided to find out.

In laboratory models, Angel and colleagues found that MG1 was able to target and eliminate latent HIV-infected cells, without harming non-infected cells. They were also able to show that MG1 successfully destroyed HIV in blood cells in a lab setting.

Angel, who is also a professor at the University of Ottawa, said he’s happy his hypothesis seems to have been correct, but he’s been surprised by how well it has held up across different experimental setups.

“What’s moreso been surprising is not so much that we saw it, but that it’s been consistently observed,” he told MD Magazine.

If the viral therapy proves successful in later rounds of study, it could serve as something of a final step in the treatment of HIV/AIDS.

Antiretroviral therapy (ART) has taken away the “death sentence” of HIV infection and, research suggests, it can also push down viral load to the point where it’s undetectable and non-transmittable. Now, MG1 holds the potential to act as a sort of knockout punch for patients on ART, destroying those latent HIV-infected cells once and for all.

“Where the opportunities lie are for people that are on effective therapy,” Angel said. “...There’s a kind of desire to cure the patients and a desire to get rid of the remaining HIV cells so therapies can be unnecessary, whether permanently or temporarily.”

Aside from the virus-versus-virus strategy, Angel said the major breakthrough in the research is the ability to identify HIV cells at a level that goes beyond a surface-level signature.

“What’s unique about this approach is not so much the virus itself but it’s targeting something within the cell that kind of distinguishes it from other cells,” he said.

As with the oncology applications of MG1, there’s still work to be done to see whether MG1 is the best virus to attack HIV, and also to determine what dosing levels might be effective without causing severe side effects. Angel said MG1 can cause fever and malaise at certain doses.

That’s not a deterrent for cancer patients enrolled in experimental trials, but he said the calculus will be different when dealing with patients who are living normal healthy lives thanks to ART.

Angel and colleagues are currently in the process of developing a clinical trial, though he said they’re still near the beginning of that long process.

In the meantime, they’ll work to test the therapy in animal models, starting with mice.

The study is titled, “The oncolytic virus, MG1, targets and eliminates latently HIV-1-infected cells: implications for an HIV cure” and was published last month in The Journal of Infectious Diseases.