New research reveals why the HIV virus remains in the human body despite successful therapies

Treatment of HIV has made great strides in the last few years with patients fully recovering from the condition due to recent therapies.

However, one thing that remains consistent is that the virus stays in the body even after a patient has successfully undergone treatment.

Now, researchers from the University of Alberta have come up with a possible answer as to why this occurs that could lead to improved therapies, according to a statement released by the institution on Friday.

Killer T cells without the CD73 protein

It all has to do with the killer T cells. These cells are a type of white blood cells responsible for identifying and destroying cells infected with viruses and, unfortunately, they lack a protein called CD73 which hinders their ability to spot and eliminate HIV-infected cells.

“This mechanism explains one potential reason for why HIV stays in human tissues forever,” said immunologist Shokrollah Elahi who lead the new research. The discovery may lead to potentially more effective therapies.

“This provides us the opportunity to come up with potential new treatments that would help killer T cells migrate better to gain access to the infected cells in different tissues," Elahi added.

But why does this decrease in CD73 occur? Elahi sought to answer that question too. This project took him three years to complete but he came up with a plausible solution.

Chronic inflammation to blame

“Following extensive studies, we discovered that chronic inflammation results in increased levels of a type of RNA found in cells and in blood, called microRNAs,” he explained. “These are very small types of RNA that can bind to messenger RNAs to block them from making CD73 protein. We found this was causing the CD73 gene to be suppressed.”

There is, however, one good aspect of a lowered presence of CD73 and that is a lowered chance of getting multiple sclerosis. Elahi and his team are therefore now investigating different methods for turning on the gene in patients with HIV and turning it off for those with multiple sclerosis.