對于寄生蟲布氏錐蟲CTP合成酶的研究使研究者離成功治愈非洲嗜睡病又近了一步。研究者使用細胞毒素acivicin使錐蟲感染的小鼠免于癥狀的發作。

因為布氏錐蟲經常改變其表面的結構，因而可避免人類對其產生免疫效應，這種寄生蟲可攻擊中樞神經系統，可導致精神紊亂、破壞睡眠、并且可最終導致死亡。由于寄生蟲侵襲病人中樞神經系統，所以沒有藥物可同時治療寄生蟲感染并防止副反應。

在Umeå大學LarsThelander教授指導的一個項目中，科學家已在先前發現寄生蟲CTP合成酶，一種產生CTP的酶類，而CTP的合成可影響寄生蟲mRNA的合成，這個過程對于寄生蟲的生存至關重要且是治療疾病的靶位點。

在最新的研究中，科學家試圖確定acivicin治療時的恰當劑量，而acivicin是一種眾所周知的細胞毒素，可作為腫瘤藥物，抑制寄生蟲CTP合成，因而最終殺滅細胞中的寄生蟲。維持日常劑量的acivicin，錐蟲感染的小鼠可以避免產生相應的癥狀，而對照組小鼠感染后幾天內就會死去。

acivicin的優勢是其已在臨床上應用于人類。所有的臨床研究對這已經確認，并且已知這種藥物可以進入中樞神經系統，明顯與其他的治療藥物有所區別。除外，它可以制成藥片，在健康醫療受限的國家來說這種藥物形式尤其重要。

Umeå大學醫學化學和生物物理學教研室的研究團隊希望找到acivicin合適的劑量以持續治療寄生蟲感染的小鼠。 


Acivicin:HopeForaCureForAfricanSleepingSickness 

Studies of the enzyme CTP synthetase in the parasite Trypanosoma brucei have brought researchers closer to a cure for African sleeping sickness. They have kept trypanosome-infected mice free of symptoms with the cell toxin acivicin.Since the parasite Trypanosoma brucei constantly changes its surface, it can avoid the immune defence of humans and invade the central nervous system, which leads to personality disturbances, sleep disruptions, and ultimately death. For patients affected by a severe Trypanosoma brucei infection in the central nervous system, there are no medicines that can treat both subspecies without incurring extremely serious side effects. 

In a project directed by Professor Lars Thelander from Umeå University, scientists have previously discovered that the parasites’ CTP synthetase, an enzyme responsible for the production of CTP - one of the four building blocks for mRNA synthesis, a process that is critical for the survival of the parasite ¬ should be a key target for treating the disease.

In the current publication scientists have managed to show that the proper content of acivicin, a well-known cell toxin that has previously been used as a cancer drug, can inhibit the parasite’s CTP synthetase, thereby permanently killing the trypanosomes in cell cultures. With daily doses of acivicin, trypanosome-infected mice have also been kept free of symptoms, as opposed to untreated mice that died within a few days.

“The advantage of acivicin is that it has already been used on humans. All the clinical studies have been performed, and we know that the drug can penetrate the central nervous system, which is not the case with many other medicines for trypanosomes. What's more, it can be taken in tablet form, which is extremely important in countries with limited health-care resources,” says Artur Fijolek from Umeå University, co-author of the article.

The research team at the Umeå University Department of Medical Chemistry and Biophysics hopes soon to be able to find the appropriate dosage of acivicin that can permanently cure the infected mice.