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Infection and Immunity, June 1999, p. 2975-2985, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

A Longitudinal Study of Human Antibody Responses to Plasmodium falciparum Rhoptry-Associated Protein 1 in a Region of Seasonal and Unstable Malaria Transmission

Peter N. Fonjungo,1,dagger Ibrahim M. Elhassan,2,3 David R. Cavanagh,1 Thor G. Theander,2 Lars Hviid,2 Cally Roper,1,4 David E. Arnot,1 and Jana S. McBride1,*

Institute of Cell, Animal and Population Biology, University of Edinburgh, Edinburgh EH9 3JT, Scotland1; Centre for Medical Parasitology at the Institute for Medical Microbiology and Immunology, University of Copenhagen and RHIMA Centre, Copenhagen University Hospital (Rigshospitalet), Copenhagen, Denmark2; Institute of Endemic Diseases, University of Khartoum, Khartoum, Sudan3; and Department of Infectious and Tropical Disease, London School of Hygiene and Tropical Medicine, London, England4

Received 26 October 1998/Returned for modification 15 December 1998/Accepted 26 March 1999

Rhoptry-associated protein 1 (RAP1) of Plasmodium falciparum is a nonpolymorphic merozoite antigen that is considered a potential candidate for a malaria vaccine against asexual blood stages. In this longitudinal study, recombinant RAP1 (rRAP1) proteins with antigenicity similar to that of P. falciparum-derived RAP1 were used to analyze antibody responses to RAP1 over a period of 4 years (1991 to 1995) of 53 individuals naturally exposed to P. falciparum malaria. In any 1 year during the study, between 23 and 39% of individuals who had malaria developed immunoglobulin G (IgG) antibodies detectable with at least one rRAP1 protein. However, the anti-RAP1 antibody responses were detected only during or shortly after clinical malarial infections. RAP1 antibody levels declined rapidly (within 1 to 2 months) following drug treatment of the infections. No anti-RAP1 antibodies were usually detected a few months after the end of malaria transmission, during the dry season, or by the start of the next malaria season. Thus, RAP1 IgG responses were very short-lived. The short duration of RAP1 antibody response may explain the apparent lack of response in a surprisingly high proportion of individuals after clinical malarial infections. For some individuals who experienced more than one malarial infection, a higher anti-RAP1 antibody response to subsequent infections than to earlier infections was observed. This suggested secondary responses to RAP1 and thus the development of immunological memory for RAP1.

* Corresponding author. Mailing address: Institute of Cell, Animal and Population Biology, University of Edinburgh, King's Buildings, West Mains Rd., Edinburgh EH9 3JT, Scotland. Phone: 44 131 650 5494. Fax: 44 131 667 3210. E-mail: JMCBRIDE{at}ed.ac.uk.

dagger Present address: HIV/Retrovirus Disease Branch, Centers for Disease Control and Prevention, Atlanta, Ga.

Infection and Immunity, June 1999, p. 2975-2985, Vol. 67, No. 6
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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