In:
eLife, eLife Sciences Publications, Ltd, Vol. 3 ( 2014-05-20)
Abstract:
African sleeping sickness is a potentially lethal disease that is caused by a parasite called T. brucei and spread by tsetse flies. Like many of the parasites that cause tropical diseases, T. brucei employs genetic trickery to evade the immune systems of humans and other mammals. This involves changing the variant surface glycoprotein (VSG) coat that surrounds the parasite on a regular basis in order to remain one step ahead of the immune system of its host: while the immune system looks for invaders wearing a particular coat, the parasites are spreading through the host in a completely different coat. To infect other hosts, the parasite must undergo changes that allow it to re-infect the tsetse fly. Therefore, besides the ‘antigenic variation’ that allows it to change its surface coat when it is in the blood of its host, T. brucei must undergo a more fundamental metamorphosis before it is capable of colonizing the tsetse fly. However, many details of the changes that allow the parasites to re-infect flies are not understood. T. brucei has several hundred VSG genes clustered in about 15 regions known as expression sites, but only a single expression site is active at any given time. Each expression site also contains a number of other genes known as expression site-associated genes (ESAGs). Antigenic variation can occur as a result of different VSG genes within the same expression site being expressed as proteins, or when the active expression site is silenced and another expression site is activated. This is another process that is not fully understood. Batram et al. now reveal that the expression of VSG genes, antigenic variation and the changes that allow the parasites to re-infect flies are all related to each other. This suggests that the expression site could provide a new point of attack in the fight against African sleeping sickness.
Type of Medium:
Online Resource
ISSN:
2050-084X
DOI:
10.7554/eLife.02324.001
DOI:
10.7554/eLife.02324.002
DOI:
10.7554/eLife.02324.003
DOI:
10.7554/eLife.02324.004
DOI:
10.7554/eLife.02324.005
DOI:
10.7554/eLife.02324.006
DOI:
10.7554/eLife.02324.007
DOI:
10.7554/eLife.02324.008
DOI:
10.7554/eLife.02324.009
DOI:
10.7554/eLife.02324.010
DOI:
10.7554/eLife.02324.011
DOI:
10.7554/eLife.02324.012
DOI:
10.7554/eLife.02324.013
DOI:
10.7554/eLife.02324.014
DOI:
10.7554/eLife.02324.015
DOI:
10.7554/eLife.02324.016
DOI:
10.7554/eLife.02324.017
DOI:
10.7554/eLife.02324.018
Language:
English
Publisher:
eLife Sciences Publications, Ltd
Publication Date:
2014
detail.hit.zdb_id:
2687154-3
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