Scientists have found that the parasite Trypanosoma brucei hides from the immune system using a protein that selectively suppresses "unnecessary” genes and directs resources toward building a protective shell. This conclusion was reached by researchers from University of York. The results of the study were published in the journal Nature Microbiology.
The parasite causes sleeping sickness — a dangerous tropical disease transmitted through the bites of the tsetse fly. It was previously known that it disguises itself using a "molecular cloak” made of variable surface glycoproteins (VSG), which constantly renews itself and makes the parasite invisible to the immune system. However, how this active defense is maintained remained unclear for more than 40 years.
Researchers identified a key element of this system — the ESB2 protein, which acts as a "molecular shredder.” It regulates protein synthesis inside the parasite: it enhances the production of protective VSG while simultaneously suppressing the production of other proteins. This allows the parasite to conserve resources and continuously renew its disguise.
Experiments showed that when ESB2 is removed, the balance is disrupted: the synthesis of auxiliary proteins sharply increases, while the effectiveness of the protective mechanism decreases. This confirms that ESB2 plays a central role in evading the immune response.
According to the scientists, targeting this protein could form the basis for new treatment methods. Disrupting its function would make the parasite more vulnerable to the immune system or lead to its death.
Sleeping sickness affects the central nervous system and can cause sleep disturbances, confusion, and coma. Despite existing treatments, they are not always effective or accessible, so this discovery may help in developing safer therapies.
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