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Infection and Immunity, December 1999, p. 6369-6374, Vol. 67, No. 12
Wellcome Trust Centre for the Epidemiology of
Infectious Disease, Department of Zoology, University of Oxford,
Oxford OX1 3PS, United Kingdom,1 and
Papua New Guinea Institute of Medical Research, Madang,
Papua New Guinea2
Received 12 March 1999/Returned for modification 1 June
1999/Accepted 17 September 1999
Why there are so few gametocytes (the transmission stage of
malaria) in the blood of humans infected with Plasmodium
spp. is intriguing. This may be due either to reproductive restraint by
the parasite or to unidentified gametocyte-specific immune-mediated clearance mechanisms. We propose another mechanism, a cross-stage immunity to Plasmodium falciparum erythrocyte membrane
protein 1 (PfEMP-1). This molecule is expressed on the surface of the erythrocyte infected with either trophozoite or early gametocyte parasites. Immunoglobulin G antibodies to PfEMP-1, expressed on both
life cycle stages, were measured in residents from an area where
malaria is endemic, Papua New Guinea. Anti-PfEMP-1 prevalence increased
with age, mirroring the decline in both the prevalence and the density
of asexual and transmission stages in erythrocytes. These data led us
to propose that immunity to PfEMP-1 may influence malaria transmission
by regulation of the production of gametocytes. This regulation may be
achieved in two ways: (i) by controlling asexual proliferation and
density and (ii) by affecting gametocyte maturation.
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Malaria Transmission and Naturally Acquired
Immunity to PfEMP-1

and
*
Corresponding author. Mailing address: WTCEID,
Department of Zoology, University of Oxford, South Parks Road, Oxford
OX1 3PS, United Kingdom. Phone: 44 1865 271247. Fax: 44 1865 281245. E-mail: karen.piper{at}ceid.ox.ac.uk.
Present address: NIAID/LPD, NIH, Bethesda, MD 20892.
Present address: University of Coventry, Coventry, United Kingdom.
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