YORK, England — Scientists have identified a previously unknown mechanism that helps the parasite responsible for African sleeping sickness evade the human immune system, according to a study published this year, offering new insight into how the organism survives in the bloodstream and spreads disease.
Researchers at the University of York and collaborating institutions reported that the parasite, known as African trypanosome, uses a protein called ESB2 to selectively destroy some of its own genetic instructions while preserving others. The findings were published in the journal Nature Microbiology and announced by the university in April.
African trypanosomes cause Human African Trypanosomiasis, commonly known as sleeping sickness, a disease transmitted by tsetse flies in parts of sub-Saharan Africa. According to the researchers, the parasite survives by covering itself with a dense layer of proteins known as variant surface glycoproteins, which help it avoid detection by the host's immune system.
The study found that ESB2 acts as what researchers described as a “molecular shredder,” destroying selected genetic messages inside the parasite while leaving intact those needed to produce its protective surface coating. Scientists said the process allows the parasite to generate large amounts of its defensive proteins while limiting production of other proteins.
“We've discovered that the parasite's secret to staying invisible isn't just what it prints, but what it chooses to redact,” senior author Dr. Joana Faria of the University of York said in a statement released with the study.
Researchers said the discovery helps explain a longstanding question in parasite biology. For decades, scientists had observed that the parasite produces disproportionately large amounts of the proteins that form its protective outer layer, but the mechanism behind that imbalance remained unclear. The newly identified role of ESB2 provides an explanation, according to the study.
The research involved scientists from several countries, including the United Kingdom, Portugal, Germany, the Netherlands, Singapore and Brazil. Funding was provided through a Sir Henry Dale Fellowship supported by the Wellcome Trust and the Royal Society, according to the University of York.
Independent experts were not quoted in the university announcement, and the study did not report an immediate clinical application. However, the researchers said understanding how the parasite regulates protein production could help identify potential vulnerabilities in its life cycle and support future treatment research.
As of June 2026, the findings add to ongoing efforts to better understand parasitic diseases that continue to affect populations in parts of Africa. Researchers said further work will be needed to determine whether the newly identified mechanism can be targeted in future therapies.
