Free-flow electrophoresis for the separation of malaria infected and uninfected mouse erythrocytes and for the isolation of free parasites (Plasmodium vinckei): A new rapid technique for the liberation of malaria parasites from their host cells

1979 ◽  
Vol 58 (2) ◽  
pp. 151-159 ◽  
Author(s):  
Hans-G. Heidrich ◽  
Lorenz Rüssmann ◽  
Bettina Bayer ◽  
Albrecht Jung

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jane M. Carlton

AbstractThe study of human malaria caused by species of Plasmodium has undoubtedly been enriched by the use of model systems, such as the rodent malaria parasites originally isolated from African thicket rats. A significant gap in the arsenal of resources of the species that make up the rodent malaria parasites has been the lack of any such tools for the fourth of the species, Plasmodium vinckei. This has recently been rectified by Abhinay Ramaprasad and colleagues, whose pivotal paper published in BMC Biology describes a cornucopia of new P. vinckei ‘omics datasets, mosquito transmission experiments, transfection protocols, and virulence phenotypes, to propel this species firmly into the twenty-first century.



Parasitology ◽  
1978 ◽  
Vol 76 (1) ◽  
pp. 55-60 ◽  
Author(s):  
F. E. G. Cox

SummaryMice which have recovered from infections with the avirulent piroplasm Babesia microti are also resistant to challenge with the virulent malaria parasite Plasmodium vinckei. In mice infected with P. vinckei before the peak of the B. microti infection the numbers of malaria parasites in the blood increase until that peak and are then eliminated at the same time as the piroplasms. In mice infected with P. vinckei at or after the peak there is no apparent multiplication and the malaria parasites begin to disappear from the blood immediately. The malaria parasites in doubly infected mice show signs of degeneration similar to those seen in mice pre-treated with Corynebacterium parvum and it is suggested that a common mechanism exists in homologous and heterologous immunity and in immunity following pre-treatment with C. parvum or BCG.



2015 ◽  
Vol 6 ◽  
Author(s):  
Hiroko Okada ◽  
Kazutomo Suzue ◽  
Takashi Imai ◽  
Tomoyo Taniguchi ◽  
Chikako Shimokawa ◽  
...  


2020 ◽  
Author(s):  
Jian Huang ◽  
Yafei Yuan ◽  
Na Zhao ◽  
Debing Pu ◽  
Qingxuan Tang ◽  
...  

AbstractArtemisinin-resistant malaria parasites have emerged and been spreading, posing a significant public health challenge. Anti-malarial drugs with novel mechanisms of action are therefore urgently needed. In this report, we exploit a “selective starvation” strategy by selectively inhibiting Plasmodium falciparum hexose transporter 1 (PfHT1), the sole hexose transporter in Plasmodium falciparum, over human glucose transporter 1 (hGLUT1), providing an alternative approach to fight against multidrug-resistant malaria parasites. Comparison of the crystal structures of human GLUT3 and PfHT1 bound to C3361, a PfHT1-specific moderate inhibitor, revealed an inhibitor binding-induced pocket that presented a promising druggable site. We thereby designed small-molecules to simultaneously block the orthosteric and allosteric pockets of PfHT1. Through extensive structure-activity relationship (SAR) studies, the TH-PF series was identified to selectively inhibit PfHT1 over GLUT1 and potent against multiple strains of the blood-stage P. falciparum. Our findings shed light on the next-generation chemotherapeutics with a paradigm-shifting structure-based design strategy to simultaneously targeting the orthosteric and allosteric sites of a transporter.Significance statementBlocking sugar uptake in P. falciparum by selectively inhibiting the hexose transporter PfHT1 kills the blood-stage parasites without affecting the host cells, indicating PfHT1 as a promising therapeutic target. Here, we report the development of novel small-molecule inhibitors that are selectively potent to the malaria parasites over human cell lines by simultaneously targeting the orthosteric and the allosteric binding sites of PfHT1. Our findings established the basis for the rational design of next-generation anti-malarial drugs.



2020 ◽  
Author(s):  
Abhinay Ramaprasad ◽  
Severina Klaus ◽  
Olga Douvropoulou ◽  
Richard Culleton ◽  
Arnab Pain

AbstractBackgroundRodent malaria parasites (RMPs) serve as tractable tools to study malaria parasite biology and host-parasite-vector interactions. Plasmodium vinckei is the most geographically widespread of the four RMP species collected in sub-Saharan Central Africa. Several P. vinckei isolates are available but relatively less characterized than other RMPs, thus hindering their use in experimental studies. We have generated a comprehensive resource for P. vinckei comprising of high-quality reference genomes, genotypes, gene expression profiles and growth phenotypes for ten P. vinckei isolates.ResultsThe P. vinckei subspecies have diverged widely from their common ancestor and have undergone genomic structural variations. The subspecies from Katanga, P. v. vinckei, has a uniquely smaller genome, a reduced multigene family repertoire and is also amenable to genetic manipulation making it an ideal parasite for reverse genetics. Comparing P. vinckei genotypes reveals region-specific selection pressures particularly on genes involved in mosquito transmission. The erythrocyte membrane antigen 1 and fam-c families have expanded considerably among the lowland forest-dwelling P. vinckei parasites. Genetic crosses can be established in P. vinckei but are limited at present by low transmission success under the experimental conditions tested in this study.ConclusionsPlasmodium vinckei isolates display a large degree of phenotypic and genotypic diversity and could serve as a resource to study parasite virulence and immunogenicity. Inclusion of P. vinckei genomes provide new insights into the evolution of RMPs and their multigene families. Amenability to genetic crossing and genetic manipulation make them also suitable for classical and functional genetics to study Plasmodium biology.



Parasitology ◽  
1974 ◽  
Vol 68 (1) ◽  
pp. 19-26 ◽  
Author(s):  
F. E. G. Cox

The malaria parasites, Plasmodium berghei yoelii and P. vinckei chabaudi, run comparable courses of infection in mice. When mice were treated with betamethasone infections with P. v. chabaudi were enhanced while those of P. b. yoelii were depressed. Antibody levels in betamethasone-treated mice infected with either P. b. yoelii or P. v. chabaudi were depressed to similar extents. The differences in parasitaemias in the two different infections are attributed to the suppression of reticulocyte production by betamethasone. P. b. yoelii preferentially invades reticulocytes and the patterns of parasitaemia follow the level of reticulocytes in the blood. P. v. chabaudi has no preference for reticulocytes and the pattern of parasitaemia is influenced by the depressed immunological response of the host.



mSphere ◽  
2021 ◽  
Author(s):  
Jan Stephan Wichers ◽  
Carolina van Gelder ◽  
Gwendolin Fuchs ◽  
Julia Mareike Ruge ◽  
Emma Pietsch ◽  
...  

Malaria parasites live and multiply inside cells. To facilitate their extremely fast intracellular proliferation, they hijack and transform their host cells.



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