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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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