Abstract
Sleeping sickness is caused by a eukaryotic unicellular parasite known to infect wild animals, cattle, and humans. It causes a fatal disease that disrupts many rhythmic physiological processes, including daily rhythms of hormonal secretion, temperature regulation, and sleep, all of which are under circadian (24-h) control. In this review, we summarize research on sleeping sickness parasite biology and the impact it has on host health. We also consider the possible evolutionary advantages of sleep and circadian deregulation for the parasite.
Highlights
Specialty section: This article was submitted to Parasite and Host, a section of the journal Frontiers in Cellular and Infection
We summarize research on sleeping sickness parasite biology and the impact it has on host health
Human African trypanosomiasis (HAT), best known as sleeping sickness, is a fatal infectious disease caused by the unicellular parasite, Trypanosoma brucei
Summary
Is usually acute, and death occurs within weeks to months (Odiit et al, 1997), possibly due to this parasite being less adapted to humans (WHO, 2013). As a whole, African trypanosomiasis still represents a serious health and socio-economic burden, and it is believed that a substantial number of human and animal infections remain unreported since the disease is endemic in rural areas (Beschin et al, 2014). Besides the severe life threat posed by sleeping sickness to humans, Nagana, causes around 3 million cattle deaths and total annual losses of US $4.75 billion. No prophylactic treatment or vaccine are available, and so far the common drugs used to treat early and late stage sleeping sickness are not orally accessible, often very toxic, and sometimes ineffective (Jacobs et al, 2011; Buscher et al, 2017; Field et al, 2017)
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