Blocking protein may ability to fight HIV: study

Scientists have discovered that blocking a protein which activates the body's immune response may actually help better combat HIV.
This is the first study to show the role that type I interferon plays in driving the body's immune destruction during HIV infection, said Scott Kitchen, associate professor at University of California, Los Angeles (UCLA).
"This finding is completely counterintuitive, because many believe that the more interferon at work, the better," said Kitchen.
"We show that the type of interferon being produced during chronic stages of HIV infection has detrimental effects on the body's ability to fight off HIV and other types of infection or cancer and could actually be contributing to accelerated HIV disease," he said.

HIV cripples the immune system by destroying immune cells called CD4 T cells, which are activated during early HIV infection by type I interferon.
CD4 T cells are also known as helper cells as they signal another type of T cell, CD8, to destroy HIV-infected cells.

HIV evades the body's CD8 cells by constantly mutating, escaping recognition by CD8 cells and making them ineffective.
The chronically heightened state of inflammation and activation eventually leads to what is known as immune exhaustion when the immune cells can no longer function properly to clear infected cells.
This, along with the loss of CD4 T cells ultimately leads to the destruction of the immune system.

The researchers' idea is to block type I interferon to reduce chronic activation of the immune cells, which could give the exhausted CD8 T cells the opportunity to restore their abilities to fighting strength.
Combine that with antiretroviral therapy and it may be possible to both restore immune function and eradicate HIV throughout the body.
The researchers used "humanised mice," which have had their immune systems replaced with human immune system cells, thymus tissue and bone marrow.
They treated HIV-infected mice with antibodies that blocked type I interferons, which allowed the mice's immune systems to revert from the state of exhaustion.

This made it possible for their immune systems to produce sufficient amounts of CD8 T cells that were primed to attack and kill HIV-infected cells.
When combined with antiretroviral therapy, the treatment accelerated the effect of antiretroviral therapy in suppressing HIV.
"We found - counterintuitively - that blocking this immune response against the virus had beneficial effects in lowering the amounts of virus and increasing the ability of the immune response to clear out the virus," said Kitchen.
More experiments are needed in non-human primates before moving on to human clinical trials to determine whether the researchers' theory holds up and this treatment is safe in humans.

The study was published in the Journal of Clinical Investigation.