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Infection and Immunity, May 2007, p. 2415-2420, Vol. 75, No. 5
0019-9567/07/$08.00+0 doi:10.1128/IAI.00951-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Thomas Lavstsen,1
Louise Turner,1
Lars Hviid,1
Anja T. R. Jensen,1 and
Thor G. Theander1
Centre for Medical Parasitology at Department of Medical Microbiology and Immunology, University of Copenhagen, and Department of Infectious Diseases, Copenhagen University Hospital (Rigshospitalet), Copenhagen, Denmark,1 National Institute for Medical Research, Tanga Centre, Tanga, Tanzania2
Received 14 June 2006/ Returned for modification 16 July 2006/ Accepted 27 January 2007
Variant surface antigens (VSA) on the surface of Plasmodium falciparum-infected red blood cells play a major role in the pathogenesis of malaria and are key targets for acquired immunity. The best-characterized VSA belong to the P. falciparum erythrocyte membrane protein 1 (PfEMP1) family. In areas where P. falciparum is endemic, parasites causing severe malaria and malaria in young children with limited immunity tend to express semiconserved PfEMP1 molecules encoded by group A var genes. Here we investigated antibody responses of Tanzanians who were 0 to 19 years old to PF11_0008, a group A PfEMP1. PF11_0008 has previously been found to be highly transcribed in a nonimmune Dutch volunteer experimentally infected with NF54 parasites. A high proportion of the Tanzanian donors had antibodies against recombinant PF11_0008 domains, and in children who were 4 to 9 years old the presence of antibodies to the PF11_0008 CIDR2ß domain was associated with reduced numbers of malaria episodes. These results indicate that homologues of PF11_0008 are present in P. falciparum field isolates and suggest that PF11_0008 CIDR2ß-reactive antibodies might be involved in protection against malaria episodes.
Published ahead of print on 5 February 2007.
Current address: Statens Serum Institute, Copenhagen, Denmark.
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