New protein discovery could lead to treatment for toxoplasmosis

The parasite toxoplasmosis could be controlled through new drug therapies thanks to the identification of a new protein. Scientists have found a new protein that reacts with other proteins and could lead to new treatments for toxoplasmosis and malaria.

Researchers from the Indiana University School of Medicine have identified a protein called GCN5b. It is an enzyme that is vital to the toxoplasma parasite's ability to replicate. This means that interfering with or blocking the protein's activities could work towards controlling the parasite and stopping it from spreading.

GCN5b is part of the molecular machinery and is involved in turning the parasite's genes off and on. It works with other proteins that have been found to be similar to those found in plants rather than humans. Dr William Sullivan, associate professor of pharmacology and toxicology, said that, as a result of this, the GCN5b enzyme is incredibly different to is human counterpart.

"That's what makes this exciting - rather than just having one enzyme that we could go after, there could be a whole collection of associated enzyme components that could be potentially targeted for drug therapies to control this parasite," he said.

By discovering the similarities between the parasite's proteins that react with GCN5b and plant proteins that function in the same way, researchers were able to fill in the missing link. This allowed them to fully explain how the parasite is able to control the turning off and on of its own genes.

It was found that by disabling the GCN5b enzyme, the parasite was unable to continue replicating, which would then stop it spreading. The protein is also present during the parasite's active and latent stages, meaning it can be targeted at all times. This means it is a promising route for drug treatment development.

Toxoplasma is also a model organism for the parasite that causes malaria, meaning this research could lead to new treatment development for the disease.