Identification of surface antigens of the asexual erythrocytic cycle of malaria parasites

1981 ◽  
Vol 9 (6) ◽  
pp. 534-534
Author(s):  
C. I. NEWBOLD
Keyword(s):  
Surface Antigens ◽  
Malaria Parasites ◽  
Erythrocytic Cycle

scholarly journals Induction of Strain-Transcending Antibodies Against Group A PfEMP1 Surface Antigens from Virulent Malaria Parasites

2012 ◽  
Vol 8 (4) ◽  
pp. e1002665 ◽  
Author(s):  
Ashfaq Ghumra ◽  
Jean-Philippe Semblat ◽  
Ricardo Ataide ◽  
Carolyne Kifude ◽  
Yvonne Adams ◽  
...  
Keyword(s):  
Surface Antigens ◽  
Malaria Parasites ◽  
Group A

scholarly journals How selection forces dictate the variant surface antigens used by malaria parasites

2011 ◽  
Vol 9 (67) ◽  
pp. 246-260 ◽  
Author(s):  
Maite Severins ◽  
Don Klinkenberg ◽  
Hans Heesterbeek
Keyword(s):  
Surface Antigens ◽  
Host Immunity ◽  
Control Measures ◽  
Limiting Factor ◽  
Malaria Parasites ◽  
Mosquito Abundance ◽  
Variant Surface Antigens ◽  
Parasite Survival ◽  
Selective Forces ◽  
High Parasitaemias

Red blood cells infected by the malaria parasite Plasmodium falciparum express variant surface antigens (VSAs) that evade host immunity and allow the parasites to persist in the human population. There exist many different VSAs and the differential expression of these VSAs is associated with the virulence (damage to the host) of the parasites. The aim of this study is to unravel the differences in the effect key selection forces have on parasites expressing different VSAs such that we can better understand how VSAs enable the parasites to adapt to changes in their environment (like control measures) and how this may impact the virulence of the circulating parasites. To this end, we have built an individual-based model that captures the main selective forces on malaria parasites, namely parasite competition, host immunity, host death and mosquito abundance at both the within- and between-host levels. VSAs are defined by the net growth rates they infer to the parasites and the model keeps track of the expression of, and antibody build-up against, each VSA in all hosts. Our results show an ordered acquisition of VSA-specific antibodies with host age, which causes a dichotomy between the more virulent VSAs that reach high parasitaemias but are restricted to young relatively non-immune hosts, and less virulent VSAs that do not reach such high parasitaemias but can infect a wider range of hosts. The outcome of a change in the parasite's environment in terms of parasite virulence depends on the exact balance between the selection forces, which sets the limiting factor for parasite survival. Parasites will evolve towards expressing more virulent VSAs when the limiting factor for parasite survival is the within-host parasite growth and the parasites are able to minimize this limitation by expressing more virulent VSAs.

Modulation of host cell receptors: a mechanism for the survival of malaria parasites

Parasitology ◽  
1997 ◽  
Vol 115 (7) ◽  
pp. 45-54 ◽  
Author(s):  
M. HOMMEL
Keyword(s):  
Endothelial Cells ◽  
Host Cell ◽  
Surface Antigens ◽  
Host Immunity ◽  
Host Cells ◽  
Microvascular Endothelial Cells ◽  
Adhesion Receptors ◽  
Malaria Parasites ◽  
Cell Receptors ◽  
Working Hypothesis

Intra-erythrocytic stages of malaria parasites can alter the surface of their host cells and release toxins which induce the production of cytokines, which in turn can up- or down-regulate the expression of adhesion receptors on the surface of microvascular endothelial cells. New adhesion receptors on endothelial cells provide the parasite with increased chances of survival despite an increasing level of host immunity. In order to take advantage of these new opportunities for survival, the parasite itself needs to make best use of its considerable ability to vary its surface antigens and adherent molecules. The paper describes the various players in this survival game and articulates a working hypothesis to explain how it may all fit together.

A pre-embedding, protein a-gold immunolabelling technique for cytocentrifuged cell monolayers for lm and tem

1986 ◽  
Vol 44 ◽  
pp. 220-221
Author(s):  
K. Chien ◽  
I.P. Shintaku ◽  
A.F. Sassoon ◽  
R.L. Van de Velde ◽  
R. Heusser
Keyword(s):  
Cell Surface ◽  
Staining Method ◽  
Protein A ◽  
Surface Antigens ◽  
Cell Suspensions ◽  
Cellular Morphology ◽  
Cellular Phenotype ◽  
Cell Surface Antigens ◽  
Cell Monolayers ◽  
Diagnostic Histopathology

Identification of cellular phenotype by cell surface antigens in conjunction with ultrastructural analysis of cellular morphology can be a useful tool in the study of biologic processes as well as in diagnostic histopathology. In this abstract, we describe a simple pre-embedding, protein A-gold staining method which is designed for cell suspensions combining the handling convenience of slide-mounted cell monolayers and the ability to evaluate specimen staining specificity prior to EM embedding.

Processing Immunoperoxidase Labeled Cell Monolayers and Cryostat Sesctions For Electron Microscopy

1985 ◽  
Vol 43 ◽  
pp. 714-715
Author(s):  
K. Chien ◽  
R. Van de Velde ◽  
I.P. Shintaku ◽  
A.F. Sassoon
Keyword(s):  
Cell Monolayer ◽  
Cell Types ◽  
Surface Antigens ◽  
Immunoperoxidase Method ◽  
Reaction Step ◽  
Hot Plate ◽  
Air Drying ◽  
New Approach ◽  
Cell Monolayers ◽  
Glass Slides

Immunoelectron microscopy of neoplastic lymphoma cells is valuable for precise localization of surface antigens and identification of cell types. We have developed a new approach in which the immunohistochemical staining can be evaluated prior to embedding for EM and desired area subsequently selected for ultrathin sectioning.A freshly prepared lymphoma cell suspension is spun onto polylysine hydrobromide- coated glass slides by cytocentrifugation and immediately fixed without air drying in polylysine paraformaldehyde (PLP) fixative. After rinsing in PBS, slides are stained by a 3-step immunoperoxidase method. Cell monolayer is then fixed in buffered 3% glutaraldehyde prior to DAB reaction. After the DAB reaction step, wet monolayers can be examined under LM for presence of brown reaction product and selected monolayers then processed by routine methods for EM and embedded with the Chien Re-embedding Mold. After the polymerization, the epoxy blocks are easily separated from the glass slides by heatingon a 100°C hot plate for 20 seconds.

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