A new study found a basic mechanism which enables the HIV virus to completely override and wipe out the body’s immune system thus resulting to “cell suicide.”
The new findings of this study could pave the way for new approaches for AIDS research and treatment. It may also find a cure for the disease affecting almost 35 million people around the globe.
The result of the study, published simultaneously in the scientific journals Science and Nature, implied that an anti-inflammatory drug could be repurposed as a viable treatment for AIDS. The experimental drug, owned by Vertex Pharmaceuticals has already been tested on people.
"Our papers deal with the fundamental issue that causes AIDS, and that is the loss of CD4 T cells," said Dr. Warner Greene from the Gladstone Institutes.
Greene added that for many years, scientists thought that HIV affects the immune system by infecting its cell directly, enabling them to hijack the DNA machinery and transforming them to cells which further produce the virus. However, the study found that this happens only in a small portion of CD4-T cells.
"The cell is committing suicide in a vain attempt to protect the host," said Greene. "The abortive process releases a call for help from new CD4 cells, who then fall victim to this fiery death."
The research team explored the effects of possibly blocking cell suicide using an anti-inflammatory drug. The drug blocks the caspse-1 enzyme, preventing the cell to destroy itself. Greene said that the drug was already tested in patients as treatment for chronic seizure. However, the results of the test were not enough to continue developing the drug.
"We would like to see if that drug could be repurposed to prevent inflammation in CD4 T cell loss in HIV infection," Greene stated.
Gladstone started a negotiation with Vertex to see if they can gain access to the drug and use it for clinical trials as a new treatment for HIV infection. Gladstone believes that the drug has a lot of potential in shedding a new light on this seemingly incurable disease.
