The African sleeping sickness is one of the several infectious diseases that are hard to treat due to their capacity to bypass the immune system. Caused by the parasite Trypanosoma brucei, the African sleeping sickness is transmitted via the bites of the tsetse flies.
It can attack the host's main organs, including the brain, the disease can disrupt sleeping patterns, thus the name. When the parasite inhabits a tsetse fly, proteins called procyclins forms. When the parasite enters a mammal's bloodstream, including humans, the parasite forms a layer of glycoproteins. The proteins constantly evolve, enabling the parasites to evade the immune system's attacks.
Researchers at the Rockefeller University found a novel way of tweaking the trypanosomes in the mammal's bloodstream. The method transforms the trypanosomes back into the fly stage status, enabling the immune system to effectively kill the parasites. The findings were published in the PLOS Biology journal on Dec. 8.
"By blocking these chromatin-interacting proteins, we have found a way to make the parasite visible to the immune system," said Laboratory of Lymphocyte Biology head Nina Papavasiliou.
Genes expressions changes when chromatin and regulatory proteins interact. A protein region called bromodomain contributes in cell variation. In the study, the researchers subdued the bromodomain by exposing it to a drug called I-BET151, which is capable of blocking the protein region. Gene expressions changed from bloodstream from to fly state. The parasites also formed the initial procyclin coating.
The findings suggest that bromodomain proteins keeps trypanosomes in their bloodstream form. Subduing the bromodomain will keep the parasite from transforming and pave the way for the illness' future treatment.
The theory was tested on mice subjects. The mice induced with I-BET151-treated trypanosomes lived longer than the control group. The lab results showed that I-BET151 diminishes the parasite's ability to invade the host mammal.
The parasites became a steady target, enabling the immune system to identity and launch an attack, explained lead study author Danae Schulz. While I-BET151 is not yet ready for clinical treatments, the study provides basis for a future drug that could treat several parasitic diseases.
