How Does The African Sleeping Virus Affect Animals And Humans

Hidden deep in the rural villages of sub-Saharan Africa, a neglected tropical affliction called African sleeping sickness kills tens of thousands of people every year. Sleeping sickness is caused by a single-celled parasite named Trypanosoma brucei, which tin infect humans and other mammals (such as cattle and deer) and is transmitted from one host to another through the bite of the tsetse fly. Overlooked for decades, researchers are at present trying to better understand both the unique biology of this important homo parasite and how T. brucei might have directed the course of human development. It seems equally though this microscopic organism has left a mark of its presence on the homo genome, which scientists are but now starting time to uncover.

Trypano-what?: Trypanosome Nuts

Trypanosomes live inside the human bloodstream, where they feast on the nutrients that normally keep us healthy. By doing then they cause fever, headaches and joint pain [1]. Eventually, some of the rapidly-multiplying trypanosomes wiggle their way across the claret-encephalon barrier, which separates the circulating blood from the fundamental nervous organisation. Once the parasites enter the central nervous organization, they can trigger changes in behavior, cause confusion and disrupt the sleep cycle (hence the proper name "sleeping sickness"). Without treatment, an infected person will likely fall into a coma and succumb to the illness, sometimes within weeks of showing the offset symptoms.

Figure 1. T. brucei (colored in bluish) shown with the red blood cells with which they coexist in the human bloodstream (red). Image credit: http://www.parasitemuseum.com/trypanosome/

African trypanosomes tin can be divided into two subspecies – 1 from East Africa (T. brucei rhodesiense) and ane from West Africa (T. brucei gambiense). For reasons nosotros don't fully sympathize, T. brucei rhodesiense causes acute disease lasting from a few weeks to months and near ever results in death, while infection with T. brucei gambiense results in chronic affliction that can last for many years and sometimes resolves without complications. Unfortunately, treatment for sleeping sickness caused by either subspecies is simply moderately effective and involves "medicines" that sometimes do more impairment than good to the infected person. Throughout much of the twentieth century, the only handling for sleeping sickness after the parasites had infected the central nervous system was a drug called Melarsoprol, which contains arsenic in its chemical structure and kills approximately ane in ten patients who take information technology [2]. To learn more about African sleeping sickness and the people affected by the disease, see the documentary pic posted at [three].

The evolutionary give and take of human-parasite relationships

So, what can this terrible affliction caused past a tiny, single-celled parasite teach united states of america nearly human evolution? Quite a chip! A report recently published in the periodical Science describes possible links betwixt differences in the Apoliprotein L1 (ApoL1) gene and kidney disease in African Americans [four]. The differences the authors found are two genetic variants within the gene that codes for ApoL1. The protein made by the ApoL1 cistron binds to lipids and forms a component of high density lipoprotein (HDL, more normally known equally "good" cholesterol). The authors discovered that the variants they found in the ApoL1 gene that are associated with kidney disease in African Americans besides seem to make the variant ApoL1 protein able to lyse (break open and impale) T. brucei rhodesiense parasites. This is an example of how mutations that have arisen in the human being genome tin can enhance the body's ability to fight off pathogens. Some other example of this is the case of sickle jail cell anemia, whereby people with genetic variants that cause sickle cell anemia are less susceptible to malaria [5]. Such survival-enhancing mutations as those constitute in ApoL1 and sickle-jail cell anemia arise through the procedure of natural selection.

To empathize the footing of development and natural choice, imagine that Nature is constantly introducing mutations in our genomes, randomly over time. These random mutations are commonly neutral (neither skillful nor bad), but in rare instances, a mutation gives an individual a comparative advantage over their peers. Mutations can be advantageous if they lead to a greater chance of survival in a item environment and reproductive success, and both of these ensure that benign mutations volition exist preserved and passed on to the adjacent generation. Conversely, deleterious mutations are removed from the "gene pool," as individuals bearing them are unable to survive too as their peers.

The authors of the ApoL1 study started with a curious observation: African Americans seem more likely to develop kidney failure than their European American counterparts. Wondering whether there is a genetic basis for this phenomenon, the authors looked for genetic variations betwixt African Americans who either did or did not have kidney affliction. It turns out that the variants they uncovered in the ApoL1 gene conferred an approximately x-fold increase in the run a risk of kidney disease; in other words, if you possessed these two variants yous would exist 10 times more probable to develop kidney disease. These variants only exist in African Americans and do not account for all cases of kidney disease, but having a mutated ApoL1 gene may be a reason for the increased disease incidence amidst people of African descent.

From an evolutionary perspective, a mutation that makes a person more likely to develop kidney disease should be "weeded" out of the population over fourth dimension, as natural selection acts upon the weakest individuals of a population to remove their gene variants from the cistron pool. Nonetheless, the authors speculate that the same genetic differences they found in the ApoL1 gene may take also given ancestral Africans an advantage against a more pressing threat — infection with T. brucei. The authors tested the ability of mutant versions of the ApoL1 poly peptide to kill T. brucei rhodesiense (the parasite that causes the astute, quick-killing version of the illness) and found that human being serum containing variant ApoL1, simply non the normal version, was able to kill the trypanosomes.

Thus, a mutation that was likely selected for its protective upshot against infection with the T. brucei parasite also seems to contribute to kidney affliction in African Americans after in life. Further piece of work is certainly needed to identify whether the ApoL1 variants identified in this study actually exist in African communities often plagued by T. brucei infection. Screening patients for these variants tin can also help guide treatment for kidney disease and might prolong the time before kidney disease turns into kidney failure. Lastly, the chase is on for other variations in the human genome that make us more or less susceptible to diverse infectious diseases, such as tuberculosis and flu. It is amazing to think most all the other ways that human pathogens may have shaped our genomes, without our knowing it.

Daria Van Tyne is a graduate student in the Department of Immunology and Infectious Diseases at the Harvard School of Public Health.

References

[1] WHO Factsheet on African trypanosomiasis (Globe Health Organization) http://www.who.int/mediacentre/factsheets/fs259/en/

[2] MSF Campaign for Access to Essential Medicines: Sleeping sickness (Medicins Sans Frontieres) http://world wide web.msfaccess.org/main/other-diseases/sleeping-sickness/

[3] Survival – The Deadliest Illness (Survival Television set and BBC Globe News) http://www.survival.television set/documentaries/sleeping_sickness.php

[4] Genovese K, Friedman DJ, Ross MD, Lecordier Fifty, Uzureau P, Freedman BI, Bowden DW, Langefeld CD, Oleksyk TK, Uscinski Knob AL, Bernhardy AJ, Hicks PJ, Nelson GW, Vanhollebeke B, Winkler CA, Kopp JB, Pays E, Pollak MR. Association of trypanolytic ApoL1 variants with kidney disease in African Americans. Science Aug thirteen 2010. 329(5993): pp. 841-v

[five] Evolution: Library: A Mutation Story (PBS) http://www.pbs.org/wgbh/evolution/library/01/2/l_012_02.html

Source: https://sitn.hms.harvard.edu/flash/2011/issue91/

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