Malaria Transmission and Naturally Acquired Immunity to PfEMP-1
AUTOR(ES)
Piper, Karen P.
FONTE
American Society for Microbiology
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=97044Documentos Relacionados
- Understanding Naturally Acquired Immunity to Plasmodium falciparum Malaria
- Phagocytosis Does Not Play a Major Role in Naturally Acquired Transmission-Blocking Immunity to Plasmodium falciparum Malaria
- Targeted mutagenesis of Plasmodium falciparum erythrocyte membrane protein 3 (PfEMP3) disrupts cytoadherence of malaria-infected red blood cells
- Naturally acquired immunity to tetanus toxin in an isolated community.
- Failure of Naturally Acquired Rhinovirus Infections to Produce Temporal Immunity to Heterologous Serotypes
