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Infection and Immunity, October 2000, p. 5856-5863, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Lack of Association between Maternal Antibody and Protection of African Infants from Malaria Infection

E. M. Riley,1,2,* G. E. Wagner,2 M. F. Ofori,3 J. G. Wheeler,1 B. D. Akanmori,3 K. Tetteh,1 D. McGuinness,2 S. Bennett,1 F. K. Nkrumah,3 R. F. Anders,4 and K. A. Koram3

Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT,1 and Institute of Cell, Animal and Population Biology, Division of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JT,2 United Kingdom; Noguchi Memorial Institute for Medical Research, University of Ghana, Legon, Ghana3; and Walter and Eliza Hall Institute of Medical Research, Royal Melbourne Hospital, Melbourne, Victoria 3050, Australia4

Received 18 May 2000/Returned for modification 29 June 2000/Accepted 26 July 2000

Maternally derived antibodies are believed to protect infants against infection, but there is little direct evidence for a protective role of passively acquired antibodies against malaria. A longitudinal study of malaria infection in 143 infants was conducted in a region of southern Ghana where Plasmodium falciparum is endemic. Infants born in the high-transmission season were less likely to become infected in the first 20 weeks of life than children born in the low-transmission season. Plasma, obtained at birth, was tested for immunoglobulin G (IgG) and IgG subclasses to P. falciparum schizonts and recombinant circumsporozoite antigen, MSP-119, MSP-2, AMA-1, and Pf155 (also called ring-infected erytrocyte surface antigen). Antibody levels at birth were not associated with resistance to malaria infection. On the contrary, antibodies at birth were positively associated with infection, indicating that high levels of maternally derived antibodies represent a marker for intensity of exposure to malaria infection in infants. However, all five children who experienced high-density infections (>100 parasites/µl of blood) were seronegative for MSP-119 at the time of infection.

* Corresponding author. Mailing address: Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel St., London WC1E 7HT, United Kingdom. Phone: (44) 207 927 2706. Fax: (44) 207 637 4314. E-mail: eleanor.riley{at}lshtm.ac.uk.

Infection and Immunity, October 2000, p. 5856-5863, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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