HIV Breakthrough Could Speed Up Cure

Over a decade since the scientific community reached a consensus that HIV cannot be cured unless its ‘reservoir cells’ are targeted, it looks like progress is finally being made towards that direction.

‘Reservoir cells’ are cells that function as ‘hosts’ to the HIV virus while a patient is undergoing therapy. This means that as long as the patient is being treated, the HIV can stay safely hidden in these ‘secret containers’, evading antiviral treatments as well as the patient’s immune response system by not expressing any viral protein. As soon as treatment stops, however, the ‘sleeping’ virus suddenly comes alive, rapidly multiplying, making the disease gain momentum and progress once again.

This is the reason why HIV patients require lifetime treatment.

To change this, the obvious approach is to target and kill these ‘reservoir cells’. And the necessary first step to achieve this goal will be to identify these cells and differentiate them from ordinary healthy cells.

As reported by a French research team from the Institut de génétique humaine (CNRS/Montpellier University), this is exactly what they were able to do — they have identified a protein that meets the criteria for being a reservoir cell marker. The protein is called CD32a and it seems to be the only type of protein present on the surface of infected cells.

Of course, the team did not arrive at this conclusion right away. After they compared healthy and infected cells and found the CD32a protein, they went on to study blood samples from 12 HIV-infected patients presently receiving treatment. They isolated the cells that had the protein, and were able to confirm that nearly all of them carried the HIV virus. Based on lab experiments, activating these cells led to the production of viruses that were capable of reinfecting healthy cells. Conversely, eradicating these cells resulted in delaying production of such infective viruses.

Although HIV today is not as deadly as it used to be, in a way at least, given the fact drugs can keep it from proliferating uncontrollably, we still can’t say we have a permanent way to get rid of it. As long as ‘reservoir cells’ exist, the virus will always have a way to attack again.

With the discovery of CD32a, there may now be a way to combat this ‘sleeping’ virus and hopefully make it ‘sleep’ for good. While more tests need to be done to validate the team’s findings, there’s renewed hope that we may be on the way to developing a more effective way to treat HIV.

As Tony Fauci, director of the US National Institute of Allergies and Infectious Disease in Bethesda, Maryland, told Nature: “I really hope this is correct. The fact that this work has been done by such competent investigators, and the data looks good, makes me optimistic.”

The findings have been published in the journal Nature on March 15, 2017. And CNRS has already filed a patent for the diagnostic and therapeutic use of CD32a.