Editing African trypanosomiasis (section)

=== African Sleeping Sickness Effect on Circadian Rhythm ===
Most organisms implement internal timing mechanisms to regulate the homeostasis of the body with the environment. These mechanisms, called [[circadian clock]]s, regulate pathways in core processes, where in mammals the primary circadian clock is the [[Suprachiasmatic nucleus|suprachiasmatic Nucleus (SCN]]). The SCN’s ability to serve as the organism's primary internal clock and send signals to adjacent clocks in order to collectively synchronize it can be affected by a variety of factors. Certain factors that induce inflammation such as viruses, bacteria, or parasites can disrupt the interactions between a cell’s circadian clock and the central pacemaker. Parasite aims to modify certain aspects of their host’s behavior in a way that favors their own survival and probability of transmission.To counteract this the internal clock on hosts' immune cells  anticipate the time of infection by the parasite and thus optimize its cellular defenses or susceptibility to getting infected. In the case of [[Trypanosoma brucei|Trypanosoma Brucei]], the parasite takes advantage of the host immune cells' dependence on rhythmic regulation; it attacks the internal clock of the cells in order to improve its survival and multiplication.

African sleeping sickness mainly disrupts the [[Sleep-wake cycle|sleep/wake cycle]] alongside body temperature and hormonal regulation. After treatment, the sleep-wake cycle is able to revert back to normal, indicating that the parasites are responsible for circadian rhythm alteration rather than neuronal damage.<ref name="Filipa2" />

Sleeping sickness disrupts both sleep timing and architecture. The underlying causes were investigated in a mouse model where ''T. brucei'' infected mice had a reduced ability to maintain [[Rapid eye movement sleep|REM sleep]] and an inability for a  homeostatic response to sleep deprivation. There were also reduced electrophysiological responses, electrical activity produced by the nervous system and heart, and behavioral changes. This presented a likelihood to ''T. brucei'' altering homeostatic adenosine signaling in addition to the inflammatory responses generated from the infection. 
<ref name="adenosine">{{Cite journal |last1=Rijo-Ferreira |first1=Filipa |last2=Bjorness |first2=Theresa E. |last3=Cox |first3=Kimberly H. |last4=Sonneborn |first4=Alex |last5=Greene |first5=Robert W. |last6=Takahashi |first6=Joseph S. |date=2020-11-25 |title=Sleeping Sickness Disrupts the Sleep-Regulating Adenosine System |journal=The Journal of Neuroscience |language=en |volume=40 |issue=48 |pages=9306–9316 |doi=10.1523/JNEUROSCI.1046-20.2020 |issn=0270-6474 |pmc=7687053 |pmid=33097636}}</ref>