Image: Dr Clovis Palmer (left) and research assistant Hugh Billings
New Burnet Institute research has identified a cancer drug that can block HIV replication.
According to study lead author, Dr Clovis Palmer, the drug, called a PI3 Kinase inhibitor, has the potential to become part of a functional HIV cure where replication is suppressed to the point where therapy or treatment is not required.
The research involved the testing of dozens of drugs that modulate glucose metabolic activity in immune cells, which are targets for HIV.
The PI3 Kinase inhibitor was found to prevent HIV from accessing the protein and glucose molecules that it requires to multiply, thereby blocking replication.
“What’s important is that this confirmed one of our new cure strategies about starving the HIV reservoir,” Dr Palmer, the Head of Burnet’s Research Laboratory for Immunometabolism, said.
“In order for cells to become infected, they have to be metabolically active and this occurs even in HIV-positive people on treatment.
“So if we can modulate or lower the metabolic activity of these immune cells, which are targets for HIV, then it will prevent them from being targets of the replicating virus.
“Even individuals with undetectable viral load have residue replication, but this drug prevents further infection of other cells.”
Dr Palmer said the research casts the PI3 Kinase inhibitor in a new light. It’s been widely acknowledged to affect metabolic activity, but never in the context of immune cells or HIV.
This is the first time this drug has been shown to significantly suppress HIV replication.
Another plus is that while many cancer drugs have some toxic side effects, the potential for toxicity is much less in drugs such as this that specifically target immune cells.
“What’s important about this particular drug is that it improves the immune function of cells that specifically target and kill HIV,” Dr Palmer said.
“So we think that it’s a double whammy where this drug prevents or limits or starves the HIV reservoir, and it improves immune function so that any residual cells that are infected can be targeted by the normal immune system to kill the virus.”
Dr Palmer said there are already new versions of this drug in development.
“It’s quite easy to re-purpose these drugs directly into clinical trials, because they are relatively safe and we have shown as well that they have anti-inflammatory properties,” he said.
“So not only will it impact the level of HIV in the body, but it will also improve inflammation in people with HIV.”
This work was done in collaboration with researchers at the Baker Institute Melbourne, Monash University, University of New South Wales, The Peter Doherty Institute for Infection and Immunity, University of California San Francisco, Instituto de Investigaciones Biomédicas en Retrovirus y SIDA, University of Buenos Aires, and AIDS Cure Research Collaborative, Pittsburgh USA.
The research was funded by the Creative and Novel Ideas in HIV research Initiative by the International AIDS Society and the NIH.