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 Red blood cell blood group A antigen level affects the ability of heparin and PfEMP1 antibodies to disrupt Plasmodium falciparum rosettes

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Pontus Hedberg ◽  
Madle Sirel ◽  
Kirsten Moll ◽  
Mpungu Steven Kiwuwa ◽  
Petter Höglund ◽  
...  
Keyword(s):  
Plasmodium Falciparum ◽  
Blood Group ◽  
Experimental Studies ◽  
Surface Antigens ◽  
Adverse Outcomes ◽  
Single Group ◽  
Flow Cytometric Assay ◽  
Blood Group A ◽  
Flow Cytometric ◽  
Group A

Abstract Background The histo-blood group ABO system has been associated with adverse outcomes in COVID-19, thromboembolic diseases and Plasmodium falciparum malaria. An integral part of the severe malaria pathogenesis is rosetting, the adherence of parasite infected red blood cells (RBCs) to uninfected RBCs. Rosetting is influenced by the host’s ABO blood group (Bg) and rosettes formed in BgA have previously been shown to be more resilient to disruption by heparin and shield the parasite derived surface antigens from antibodies. However, data on rosetting in weak BgA subgroups is scarce and based on investigations of relatively few donors. Methods An improved high-throughput flow cytometric assay was employed to investigate rosetting characteristics in an extensive panel of RBC donor samples of all four major ABO Bgs, as well as low BgA expressing samples. Results All non-O Bgs shield the parasite surface antigens from strain-specific antibodies towards P. falciparum erythrocyte membrane protein 1 (PfEMP1). A positive correlation between A-antigen levels on RBCs and rosette tightness was observed, protecting the rosettes from heparin- and antibody-mediated disruption. Conclusions These results provide new insights into how the ABO Bg system affects the disease outcome and cautions against interpreting the results from the heterogeneous BgA phenotype as a single group in epidemiological and experimental studies. Graphical Abstract

scholarly journals Blood Lead Influences the Anemia Status of Malaria-Infected Children in Katanga Kampala Uganda

2019 ◽  
Author(s):  
Ambrose Mukisa ◽  
Denis Kasozi ◽  
Claire Aguttu ◽  
Peter C. Vuzi ◽  
Florence Nantaba ◽  
...  
Keyword(s):  
Aminolevulinic Acid ◽  
Venous Blood ◽  
Agricultural Practices ◽  
Blood Lead ◽  
P Value ◽  
Study Group ◽  
Malaria Parasites ◽  
Blood Samples ◽  
Group A ◽  
Low Levels

Lead pollutants mainly from urban agricultural practices, Leaded paints, Leaded fuels spillages, Lead-contaminated air, soils, and water sources pause a health threat to urban children in Uganda. Prolonged Lead exposure affects iron metabolism, by competitively blocking iron absorption leading to anemia. Blood Lead (BL) inhibits key enzymes ferrochelatase and aminolevulinic acid dehydrogenase (ALAD) involved in hemoglobin (Hb) biosynthesis even at very low levels. Lead poisoning and malaria infection geographically overlap, and both produce similar hematological outcome especially in children. Malaria parasites cause anemia by destroying parasitized red blood cells, therefore, co-existence of BL and malaria parasites infection worsens the anemia status of the host. This study aimed at expounding the extent of heme synthesis inhibition by BL levels among a study group of malaria positive children by measuring levels of free erythrocyte protoporphyrin (FEP) in blood samples. Briefly venous blood samples from 198 children were analyzed for malaria parasite densities by the thick smear method, hemoglobin (Hb) concentrations determined by the standard cyan methemoglobin method, BLL were analyzed on an atomic absorption spectrophotometer and FEP levels were fluorometrically measured. The results showed means of BLL (9.3 µg/dL), Hb (7.5 g/dL), FEP/Hb (8.3 µg/g) and parasite density (PD) (3.21×103 parasites / µL) among the study group. A majority of 151/198 (76.3%) of the children were moderately anemic while 8/198 (4%) were severely anemic. There was weak correlation between PD and Hb (R²= -0.15, P-value < 0.001), as compared to one between FEP/Hb and Hb (R²= -0.6, P-value=0.001). The study concludes that BL is a significant contributor to malaria anemia and should be considered in the management of anemia in malaria-endemic areas.

scholarly journals FACTORS AFFECTING THE CHAIN LENGTH OF GROUP A STREPTOCOCCI

1960 ◽  
Vol 112 (4) ◽  
pp. 687-698 ◽  
Author(s):  
Richard D. Ekstedt ◽  
Gene H. Stollerman
Keyword(s):  
Surface Antigens ◽  
M Protein ◽  
Specific Inhibition ◽  
Group A Streptococci ◽  
Factors Affecting ◽  
Low Concentrations ◽  
Group A ◽  
Virulent Group ◽  
Long Chain ◽  
Long Chains

Minute amounts of M protein were detected in culture supernates of virulent Group A streptococci by type-specific inhibition of the long chain and the bactericidal tests for anti-M antibody. The amount of M protein that was detected by the inhibition of these biological systems was less than could be demonstrated by precipitation tests. All strains of streptococci rich in M protein which were studied formed long chains when grown in sufficient concentrations of anti-M antibody. Very low concentrations of anti-M antibody escaped detection by the long chain test when strains of excessive M protein content were employed. Under such conditions the bactericidal test detected anti-M antibody more sensitively than the long chain test owing to the smaller inoculum employed in the former method. The scission of streptococcal chains may be inhibited by union of antibodies with surface antigens other than M protein. Long chains were formed when M-negative, R-positive strains were grown in sera containing anti-R antibody.

scholarly journals Type-specific antigens of group A Neisseria meningitidis: lipopolysaccharide and heat-modifiable outer membrane proteins

1980 ◽  
Vol 28 (2) ◽  
pp. 451-458 ◽  
Author(s):  
W D Zollinger ◽  
R E Mandrell
Keyword(s):  
Membrane Proteins ◽  
Membrane Protein ◽  
Neisseria Meningitidis ◽  
Outer Membrane ◽  
Outer Membrane Protein ◽  
Solid Phase ◽  
Outer Membrane Proteins ◽  
Surface Antigens ◽  
Protein Antigens ◽  
Group A

The solid-phase radioimmunoassay inhibition method was used to analyze the noncapsular surface antigens of group A Neisseria meningitidis for type specificity. By use of antisera prepared against group A strains, three serologically distinct lipopolysaccharide antigens and five outer membrane protein antigens were identified among group A strains from a variety of geographical origins. Two of the lipopolysaccharide antigens were unique to group A strains while the third was similar to those on strains of other meningococcal serogroups. Fractionation of outer membrane proteins in the presence of 2% sodium deoxycholate followed by quantitative inhibition of the typing reactions with the subfractions revealed that the protein responsible for type specificity was not the principal outer membrane protein, but, most likely, the 31,000-dalton, heat-modifiable outer membrane protein. Thus, although group A strains may share a common principal outer membrane protein, typing is feasible using other surface antigens. In a survey of 82 group A strains, 93% were typable with respect to outer membrane proteins.

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.

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