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Eukaryotic Cell, February 2003, p. 84-94, Vol. 2, No. 1
1535-9778/03/$08.00+0 DOI: 10.1128/EC.2.1.84-94.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
Matthias Homann,1 and H. Ulrich Göringer1*
Department of Microbiology and Genetics, Darmstadt University of Technology, 64287 Darmstadt,1 Department of Molecular Biology and Biochemistry, Molecular Cell Biology Unit, Free University of Berlin, 12203 Berlin, Germany2
Received 22 April 2002/ Accepted 4 October 2002
African trypanosomes cause sleeping sickness in humans and Nagana in cattle. The parasites multiply in the blood and escape the immune response of the infected host by antigenic variation. Antigenic variation is characterized by a periodic change of the parasite protein surface, which consists of a variant glycoprotein known as variant surface glycoprotein (VSG). Using a SELEX (systematic evolution of ligands by exponential enrichment) approach, we report the selection of small, serum-stable RNAs, so-called aptamers, that bind to VSGs with subnanomolar affinity. The RNAs are able to recognize different VSG variants and bind to the surface of live trypanosomes. Aptamers tethered to an antigenic side group are capable of directing antibodies to the surface of the parasite in vitro. In this manner, the RNAs might provide a new strategy for a therapeutic intervention to fight sleeping sickness.
Present address: Department Biology I, Genetics, Ludwig-Maximilians-University, 80638 Munich, Germany.
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