Plasmodium falciparum: The human agglutinating antibody response to the infected red cell surface is predominantly variant specific

1992 ◽  
Vol 75 (3) ◽  
pp. 281-292 ◽  
Author(s):  
C.I. Newbold ◽  
R. Pinches ◽  
D.J. Roberts ◽  
K. Marsh
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Antibody Response ◽  
Red Cell

scholarly journals Analysis of Immunity to Febrile Malaria in Children That Distinguishes Immunity from Lack of Exposure

2009 ◽  
Vol 77 (5) ◽  
pp. 1917-1923 ◽  
Author(s):  
Philip Bejon ◽  
George Warimwe ◽  
Claire L. Mackintosh ◽  
Margaret J. Mackinnon ◽  
Sam M. Kinyanjui ◽  
...  
Keyword(s):  
Cell Surface ◽  
Antibody Response ◽  
Observational Studies ◽  
Asymptomatic Infection ◽  
Bed Nets ◽  
Bed Net ◽  
Red Cell ◽  
Vaccine Trials ◽  
Net Use ◽  
Malaria Episodes

ABSTRACT In studies of immunity to malaria, the absence of febrile malaria is commonly considered evidence of “protection.” However, apparent “protection” may be due to a lack of exposure to infective mosquito bites or due to immunity. We studied a cohort that was given curative antimalarials before monitoring began and documented newly acquired asymptomatic parasitemia and febrile malaria episodes during 3 months of surveillance. With increasing age, there was a shift away from febrile malaria to acquiring asymptomatic parasitemia, with no change in the overall incidence of infection. Antibodies to the infected red cell surface were associated with acquiring asymptomatic infection rather than febrile malaria or remaining uninfected. Bed net use was associated with remaining uninfected rather than acquiring asymptomatic infection or febrile malaria. These observations suggest that most uninfected children were unexposed rather than “immune.” Had they been immune, we would have expected the proportion of uninfected children to rise with age and that the uninfected children would have been distinguished from children with febrile malaria by the protective antibody response. We show that removing the less exposed children from conventional analyses clarifies the effects of immunity, transmission intensity, bed nets, and age. Observational studies and vaccine trials will have increased power if they differentiate between unexposed and immune children.

scholarly journals Scanning electron microscope-analysis of the protrusions (knobs) present on the surface of Plasmodium falciparum-infected erythrocytes.

1983 ◽  
Vol 97 (3) ◽  
pp. 795-802 ◽  
Author(s):  
J Gruenberg ◽  
D R Allred ◽  
I W Sherman
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Parasite Development ◽  
Red Cell ◽  
Schizont Stage ◽  
Dynamic Changes ◽  
Trophozoite Stage ◽  
Parasite Plasmodium Falciparum ◽  
Surface Patterns ◽  
Scanning Electron

The nature of the surface deformations of erythrocytes infected with the human malaria parasite Plasmodium falciparum was analyzed using scanning electron microscopy at two stages of the 48-h parasite maturation cycle. Infected cells bearing trophozoite-stage parasites (24-36 h) had small protrusions (knobs), with diameters varying from 160 to 110 nm, and a density ranging from 10 to 35 knobs X micron-2. When parasites were fully mature (schizont stage, 40-44 h), knob size decreased (100-70 nm), whereas density increased (45-70 knobs X micron-2). Size and density of the knobs varied inversely, suggesting that knob production (a) occurred throughout intraerythrocytic parasite development from trophozoite to schizont and (b) was related to dynamic changes of the erythrocyte membrane. Variation in the distribution of the knobs over the red cell surface was observed during parasite maturation. At the early trophozoite stage of parasite development, knobs appeared to be formed in particular domains of the cell surface. As the density of knobs increased and they covered the entire cell surface, their lateral distribution was dispersive (more-than-random); this was particularly evident at the schizont stage. Regional surface patterns of knobs (rows, circles) were seen throughout parasite development. The nature of the dynamic changes that occurred at the red cell surface during knob formation, as well as the nonrandom distribution of knobs, suggested that the red cell cytoskeleton may have played a key role in knob formation and patterning.

scholarly journals Allelic Diversity of the Plasmodium falciparum Erythrocyte Membrane Protein 1 Entails Variant-Specific Red Cell Surface Epitopes

PLoS ONE ◽  
2011 ◽  
Vol 6 (1) ◽  
pp. e16544 ◽  
Author(s):  
Inès Vigan-Womas ◽  
Micheline Guillotte ◽  
Alexandre Juillerat ◽  
Cindy Vallieres ◽  
Anita Lewit-Bentley ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Membrane Protein ◽  
Cell Surface ◽  
Erythrocyte Membrane ◽  
Allelic Diversity ◽  
Red Cell ◽  
Erythrocyte Membrane Protein ◽  
Falciparum Erythrocyte Membrane Protein

Red cell surface changes and erythrophagocytosis in children with severe Plasmodium falciparum anemia

Blood ◽  
2000 ◽  
Vol 95 (4) ◽  
pp. 1481-1486 ◽  
Author(s):  
John N. Waitumbi ◽  
Malachi O. Opollo ◽  
Richard O. Muga ◽  
Ambrose O. Misore ◽  
José A. Stoute
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Red Cells ◽  
Regulatory Proteins ◽  
Severe Anemia ◽  
Red Cell ◽  
Complement Regulatory Proteins ◽  
Asymptomatic Children ◽  
Cell Surface Changes

Severe anemia is one of the most lethal complications in children infected with Plasmodium falciparum. The pathogenesis of this anemia is not completely understood. Experimental data from malaria-infected humans and animal models suggest that uninfected red cells have a shortened life span. This study looked for changes in the red cell surfaces of children with severe malarial anemia that could explain this accelerated destruction. A prospective case-control study was conducted of children with severe P falciparum anemia (hemoglobin of 5 g/dL or lower) admitted to a large general hospital in western Kenya. Children with severe anemia were compared with children who had symptoms of uncomplicated malaria and with asymptomatic children. Cytofluorometry was used to quantify in vitro erythrophagocytosis and to measure red cell surface immunoglobulin G (IgG) and the complement regulatory proteins CR1, CD55, and CD59. Red cells from patients with severe anemia were more susceptible to phagocytosis and also showed increased surface IgG and deficiencies in CR1 and CD55 compared with controls. Red cell surface CD59 was elevated in cases of severe anemia compared with asymptomatic controls but not as compared with symptomatic controls. The surface of red cells of children with severe P falciparum anemia is modified by the deposition of IgG and alterations in the levels of complement regulatory proteins. These changes could contribute to the accelerated destruction of red cells in these patients by mechanisms such as phagocytosis or complement-mediated lysis.

Plasmodium falciparum: Pathogenesis, polymorphism and the infected red cell surface

1999 ◽  
Vol 6 (1) ◽  
pp. 57-60 ◽  
Author(s):  
C Newbold ◽  
A. Craig ◽  
S. Kyes ◽  
A. Rowe ◽  
D. Fernandez-Reyes ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Red Cell

Cytoadherence, pathogenesis and the infected red cell surface in Plasmodium falciparum

1999 ◽  
Vol 29 (6) ◽  
pp. 927-937 ◽  
Author(s):  
Chris Newbold ◽  
Alister Craig ◽  
Sue Kyes ◽  
Alex Rowe ◽  
Delmiro Fernandez-Reyes ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Cell Surface ◽  
Red Cell

Functions of red cell surface proteins

Vox Sanguinis ◽  
2007 ◽  
Vol 0 (0) ◽  
pp. 070807042627006-??? ◽  
Author(s):  
G. Daniels
Keyword(s):  
Cell Surface ◽  
Surface Proteins ◽  
Red Cell ◽  
Cell Surface Proteins

scholarly journals THE ELECTROPHORETIC MOBILITY OF HUMAN ERYTHROCYTES—WHOLE CELLS, GHOSTS, AND FRAGMENTS

1938 ◽  
Vol 22 (1) ◽  
pp. 1-5 ◽  
Author(s):  
W. H. Byler ◽  
H. M. Rozendaal
Keyword(s):  
Cell Surface ◽  
Electrophoretic Mobility ◽  
Human Erythrocytes ◽  
Red Cell ◽  
Chicken Serum ◽  
Whole Cells ◽  
Slow Change ◽  
Foreign Substance ◽  
Pure Salt

The electrophoretic mobility of human red cell ghosts decreases in the presence of chicken serum. The decrease is not directly due to the presence of adsorbed material but to a change which is catalyzed by the foreign substance. It is suggested that abnormal serum materials resulting from disease may serve as catalysts. Fragments of broken cells have the same mobility as whole cells at first, then decrease even in pure salt suspension, while the whole cells remain essentially unchanged for hours. The results suggest that the slow change of whole cells, the change of ghosts in the presence of foreign serum, and the change of fragments are all manifestations of the same modification of structure or composition of the cell surface.

Protective antigens of bloodstage Plasmodium knowlesi parasites

1984 ◽  
Vol 307 (1131) ◽  
pp. 159-169 ◽  
Keyword(s):  
Monoclonal Antibodies ◽  
Cell Surface ◽  
Plasmodium Knowlesi ◽  
Surface Antigens ◽  
Red Cell ◽  
Cell Surface Antigens ◽  
Susceptible Host ◽  
Protective Antigens ◽  
Stage Of Development

The simian malaria Plasmodium knowlesi provides many favourable features as an experimental model; it can be grown in vivo or in vitro . Parasites of defined variant specificity and stage of development are readily obtained and both the natural host and a highly susceptible host are available for experimental infection and vaccination trials. Proteins synthesized by erythrocytic P. knowlesi parasites are characteristic of the developmental stage, as are the alterations that the parasite induces in the red cell surface. Erythrocytic merozoites are anatomically and biochemically complex, their surface alone is covered by at least eight distinct polypeptides. Immune serum from merozoite-immunized rhesus recognizes many parasite components, especially those synthesized by schizonts. All of the merozoite surface components and some of the schizont-infected red cell surface antigens are recognized by such immune sera. Rhesus monkeys rendered immune by repeated infection may by contrast recognize comparatively few antigens; a positive correlation was established for these ‘ naturally ’ immunized monkeys between protection and antibody directed against a 74000 molecular mass antigen. Im m unization with this purified antigen confers partial protection. O ther putative protective antigens have been identified by monoclonal antibodies that inhibit merozoite invasion of red cells in vitro . The antigens recognized by inhibitory monoclonal antibodies are synthesized exclusively by schizonts and are processed, at the time ofschizont rupture and merozoite release, to smaller molecules that are present on the merozoite surface. The multiplicity of protective antigens is clearly demonstrated by the fact that seven distinct merozoite surface antigens are recognized by three different inhibitory monoclonals. None of the protective antigens identified are variant or strain specific.

Actomyosin motor in the merozoite of the malaria parasite, Plasmodium falciparum: implications for red cell invasion

1998 ◽  
Vol 111 (13) ◽  
pp. 1831-1839 ◽  
Author(s):  
J.C. Pinder ◽  
R.E. Fowler ◽  
A.R. Dluzewski ◽  
L.H. Bannister ◽  
F.M. Lavin ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Plasma Membrane ◽  
Toxoplasma Gondii ◽  
Malaria Parasite ◽  
Cellular Protein ◽  
Red Cell ◽  
Parasite Protein ◽  
Ionic Detergent ◽  
Parasite Plasmodium ◽  
Parasite Plasmodium Falciparum

The genome of the malaria parasite, Plasmodium falciparum, contains a myosin gene sequence, which bears a close homology to one of the myosin genes found in another apicomplexan parasite, Toxoplasma gondii. A polyclonal antibody was generated against an expressed polypeptide of molecular mass 27,000, based on part of the deduced sequence of this myosin. The antibody reacted with the cognate antigen and with a component of the total parasite protein on immunoblots, but not with vertebrate striated or smooth muscle myosins. It did, however, recognise two components in the cellular protein of Toxoplasma gondii. The antibody was used to investigate stage-specificity of expression of the myosin (here designated Pf-myo1) in P. falciparum. The results showed that the protein is synthesised in mature schizonts and is present in merozoites, but vanishes after the parasite enters the red cell. Pf-myo1 was found to be largely, though not entirely, associated with the particulate parasite cell fraction and is thus presumably mainly membrane bound. It was not solubilised by media that would be expected to dissociate actomyosin or myosin filaments, or by non-ionic detergent. Immunofluorescence revealed that in the merozoite and mature schizont Pf-myo1 is predominantly located around the periphery of the cell. Immuno-gold electron microscopy also showed the presence of the myosin around almost the entire parasite periphery, and especially in the region surrounding the apical prominence. Labelling was concentrated under the plasma membrane but was not seen in the apical prominence itself. This suggests that Pf-myo1 is associated with the plasma membrane or with the outer membrane of the subplasmalemmal cisterna, which forms a lining to the plasma membrane, with a gap at the apical prominence. The results lead to a conjectural model of the invasion mechanism.

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