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Journal articles on the topic 'Plasmodium parasite'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 February 2022

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1

Gutiérrez-López, Rafael, Josué Martínez-de la Puente, Laura Gangoso, Ramón Soriguer, and Jordi Figuerola. "Plasmodium transmission differs between mosquito species and parasite lineages." Parasitology 147, no. 4 (2020): 441–47. http://dx.doi.org/10.1017/s0031182020000062.

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AbstractFactors such as the particular combination of parasite–mosquito species, their co-evolutionary history and the host's parasite load greatly affect parasite transmission. However, the importance of these factors in the epidemiology of mosquito-borne parasites, such as avian malaria parasites, is largely unknown. Here, we assessed the competence of two mosquito species [Culex pipiens and Aedes (Ochlerotatus) caspius], for the transmission of four avian Plasmodium lineages (Plasmodium relictum SGS1 and GRW11 and Plasmodium cathemerium-related lineages COLL1 and PADOM01) naturally infectin

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HANADA, Kentaro, Toshihide MITAMURA, Masayoshi FUKASAWA, Pamela A. MAGISTRADO, Toshihiro HORII, and Masahiro NISHIJIMA. "Neutral sphingomyelinase activity dependent on Mg2+ and anionic phospholipids in the intraerythrocytic malaria parasite Plasmodium falciparum." Biochemical Journal 346, no. 3 (2000): 671–77. http://dx.doi.org/10.1042/bj3460671.

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Sphingolipid metabolism and metabolites are important in various cellular events in eukaryotes. However, little is known about their function in plasmodial parasites. Here we demonstrate that neutral sphingomyelinase (SMase) involved in the sphingomyelin (SM) catabolism is retained by the intraerythrocytic parasite Plasmodium falciparum. When assayed in a neutral pH buffer supplemented with Mg2+ and phosphatidylserine, an activity for the release of the phosphocholine group from SM was detected in parasite-infected, but not in uninfected, erythrocyte ghosts. The SMase activity in the parasite-

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Tewari, Rita, Solabomi A. Ogun, Ruwani S. Gunaratne, Andrea Crisanti, and Anthony A. Holder. "Disruption of Plasmodium berghei merozoite surface protein 7 gene modulates parasite growth in vivo." Blood 105, no. 1 (2005): 394–96. http://dx.doi.org/10.1182/blood-2004-06-2106.

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Abstract Merozoite invasion of red blood cells is crucial to the development of the parasite that causes malaria. Merozoite surface proteins (MSPs) mediate the first interaction between parasite and erythrocyte. In Plasmodium falciparum, they include a complex of products from at least 3 genes (msp1, msp6, and msp7), one of which, msp7, is part of a gene family containing 3 and 6 adjacent members in Plasmodium yoelii and Plasmodium falciparum, respectively. We have identified and disrupted msp7 in the Plasmodium berghei gene family. The protein is expressed in schizonts and colocalizes with MS

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4

Antinori, Spinello, Laura Galimberti, Laura Milazzo, and Mario Corbellino. "BIOLOGY OF HUMAN MALARIA PLASMODIA INCLUDING PLASMODIUM KNOWLESI." Mediterranean Journal of Hematology and Infectious Diseases 4, no. 1 (2012): e2012013. http://dx.doi.org/10.4084/mjhid.2012.013.

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Malaria is a vector-borne infection caused by unicellular parasite of the genus Plasmodium. Plasmodia are obligate intracellular parasites that in humans after a clinically silent replication phase in the liver are able to infect and replicate within the erythrocytes. Four species (P.falciparum, P.malariae, P.ovale and P.vivax) are traditionally recognized as responsible of natural infection in human beings but the recent upsurge of P.knowlesi malaria in South-East Asia has led clinicians to consider it as the fifth human malaria parasite. Recent studies in wild-living apes in Africa have reve

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Wulandari, Diah Anggraini, and Muhammad Safaat. "REVIEW: PERAN NANOPARTIKEL DALAM MENGHAMBAT PERTUMBUHAN PARASIT Plasmodium PENYEBAB MALARIA." Jurnal Bioteknologi & Biosains Indonesia (JBBI) 8, no. 1 (2021): 124–36. http://dx.doi.org/10.29122/jbbi.v8i1.4503.

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Review: The Role of Nanoparticles in Inhibiting the Growth of the Plasmodium Parasite Causing Malarial Disease Malaria is a health problem in Indonesia with the most cases in eastern parts of Indonesia. This study provides an overview of the potential of nanoparticles in inhibiting malaria vectors and the growth of Plasmodium parasites that causes malaria based on the latest literature as reference materials and future research ideas. Nanoparticle can be synthesized using three methods i.e. physical, chemical and biological synthesis. The use of nanoparticles with biological method is highly r

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Smith, Lauren M., Francis C. Motta, Garima Chopra, et al. "An intrinsic oscillator drives the blood stage cycle of the malaria parasite Plasmodium falciparum." Science 368, no. 6492 (2020): 754–59. http://dx.doi.org/10.1126/science.aba4357.

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The blood stage of the infection of the malaria parasite Plasmodium falciparum exhibits a 48-hour developmental cycle that culminates in the synchronous release of parasites from red blood cells, which triggers 48-hour fever cycles in the host. This cycle could be driven extrinsically by host circadian processes or by a parasite-intrinsic oscillator. To distinguish between these hypotheses, we examine the P. falciparum cycle in an in vitro culture system and show that the parasite has molecular signatures associated with circadian and cell cycle oscillators. Each of the four strains examined h

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7

Galinski, Mary R. "Functional genomics of simian malaria parasites and host–parasite interactions." Briefings in Functional Genomics 18, no. 5 (2019): 270–80. http://dx.doi.org/10.1093/bfgp/elz013.

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AbstractTwo simian malaria parasite species, Plasmodium knowlesi and Plasmodium cynomolgi, cause zoonotic infections in Southeast Asia, and they have therefore gained recognition among scientists and public health officials. Notwithstanding, these species and others including Plasmodium coatneyi have served for decades as sources of knowledge on the biology, genetics and evolution of Plasmodium, and the diverse ramifications and outcomes of malaria in their monkey hosts. Experimental analysis of these species can help to fill gaps in knowledge beyond what may be possible studying the human mal

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8

Collins, William E., and Geoffrey M. Jeffery. "Plasmodium malariae: Parasite and Disease." Clinical Microbiology Reviews 20, no. 4 (2007): 579–92. http://dx.doi.org/10.1128/cmr.00027-07.

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SUMMARY A review of the life history of Plasmodium malariae, the quartan malaria parasite of humans, is presented. Much of the information is based on data obtained from induced infections in humans who were given malaria therapy for the treatment of neurosyphilis between 1940 and 1963. Prepatent periods (i.e., the time until the first day of parasite detection) fever episodes, and maximum parasitemias as a result of infection with P. malariae were obtained and are presented. Experimental and known vectors of the parasite are also discussed. Splenectomized chimpanzees and New World monkeys are

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Amin Siddiq Sumi, Hanung Adi Nugroho, and Rudy Hartanto. "A Systematic Review on Automatic Detection of Plasmodium Parasite." International Journal of Engineering and Technology Innovation 11, no. 2 (2021): 103–21. http://dx.doi.org/10.46604/ijeti.2021.6094.

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Plasmodium parasite is the main cause of malaria which has taken many lives. Some research works have been conducted to detect the Plasmodium parasite automatically. This research aims to identify the development of current research in the area of Plasmodium parasite detection. The research uses a systematic literature review (SLR) approach comprising three stages, namely planning, conducting, and reporting. The search process is based on the keywords which were determined in advance. The selection process involves the inclusion and exclusion criteria. The search yields 45 literatures from fiv

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10

Simão-Gurge, Raquel M., Neha Thakre, Jessica Strickland, et al. "Activation of Anopheles stephensi Pantothenate Kinase and Coenzyme A Biosynthesis Reduces Infection with Diverse Plasmodium Species in the Mosquito Host." Biomolecules 11, no. 6 (2021): 807. http://dx.doi.org/10.3390/biom11060807.

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Malaria parasites require pantothenate from both human and mosquito hosts to synthesize coenzyme A (CoA). Specifically, mosquito-stage parasites cannot synthesize pantothenate de novo or take up preformed CoA from the mosquito host, making it essential for the parasite to obtain pantothenate from mosquito stores. This makes pantothenate utilization an attractive target for controlling sexual stage malaria parasites in the mosquito. CoA is synthesized from pantothenate in a multi-step pathway initiated by the enzyme pantothenate kinase (PanK). In this work, we manipulated A. stephensi PanK acti

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Krogstad, D. J., P. H. Schlesinger, and I. Y. Gluzman. "Antimalarials increase vesicle pH in Plasmodium falciparum." Journal of Cell Biology 101, no. 6 (1985): 2302–9. http://dx.doi.org/10.1083/jcb.101.6.2302.

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The asexual erythrocytic stage of the malarial parasite ingests and degrades the hemoglobin of its host red cell. To study this process, we labeled the cytoplasm of uninfected red cells with fluorescein-dextran, infected those cells with trophozoite- and schizont-rich cultures of Plasmodium falciparum, and harvested them 110-120 h later in the trophozoite stage. After lysis of the red cell cytoplasm with digitonin, the only fluorescence remaining was in small (0.5-0.9 micron) vesicles similar to the parasite's food vacuole. As measured by spectrofluorimetry, the pH of these vesicles was acid (

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12

Collins, William E., and Geoffrey M. Jeffery. "Plasmodium ovale: Parasite and Disease." Clinical Microbiology Reviews 18, no. 3 (2005): 570–81. http://dx.doi.org/10.1128/cmr.18.3.570-581.2005.

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SUMMARY Humans are infected by four recognized species of malaria parasites. The last of these to be recognized and described is Plasmodium ovale. Like the other malaria parasites of primates, this parasite is only transmitted via the bites of infected Anopheles mosquitoes. The prepatent period in the human ranges from 12 to 20 days. Some forms in the liver have delayed development, and relapse may occur after periods of up to 4 years after infection. The developmental cycle in the blood lasts approximately 49 h. An examination of records from induced infections indicated that there were an av

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Kalanon, Ming, and Geoffrey I. McFadden. "Malaria, Plasmodium falciparum and its apicoplast." Biochemical Society Transactions 38, no. 3 (2010): 775–82. http://dx.doi.org/10.1042/bst0380775.

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Malaria, which is caused by species of the parasite genus Plasmodium, remains a major global health problem. A vestigial plastid homologous with the chloroplasts of plants and algae was discovered in malaria and related parasites from the phylum Apicomplexa and has radically changed our view of the evolutionary origins of these disease-causing protists. We now recognize that this large group of parasites had a photosynthetic ancestry and were converted into parasitism early in the evolution of animals. Apicomplexans have probably been parasitizing the animal kingdom for more than 500 million y

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Langhorne, Jean, and Patrick E. Duffy. "Expanding the antimalarial toolkit: Targeting host–parasite interactions." Journal of Experimental Medicine 213, no. 2 (2016): 143–53. http://dx.doi.org/10.1084/jem.20151677.

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Recent successes in malaria control are threatened by drug-resistant Plasmodium parasites and insecticide-resistant Anopheles mosquitoes, and first generation vaccines offer only partial protection. New research approaches have highlighted host as well as parasite molecules or pathways that could be targeted for interventions. In this study, we discuss host–parasite interactions at the different stages of the Plasmodium life cycle within the mammalian host and the potential for therapeutics that prevent parasite migration, invasion, intracellular growth, or egress from host cells, as well as p

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BESTEIRO, S., S. VO DUY, C. PERIGAUD, I. LEFEBVRE-TOURNIER, and H. J. VIAL. "Exploring metabolomic approaches to analyse phospholipid biosynthetic pathways in Plasmodium." Parasitology 137, no. 9 (2010): 1343–56. http://dx.doi.org/10.1017/s0031182009991934.

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SUMMARYPlasmodium falciparum, the agent responsible for malaria, is an obligate intracellular protozoan parasite. For proliferation, differentiation and survival, it relies on its own protein-encoding genes, as well as its host cells for nutrient sources. Nutrients and subsequent metabolites are required by the parasites to support their high rate of growth and replication, particularly in the intra-erythrocytic stages of the parasite that are responsible for the clinical symptoms of the disease. Advances in mass spectrometry have improved the analysis of endogenous metabolites and enabled a g

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Lisk, Godfrey, and Sanjay A. Desai. "The Plasmodial Surface Anion Channel Is Functionally Conserved in Divergent Malaria Parasites." Eukaryotic Cell 4, no. 12 (2005): 2153–59. http://dx.doi.org/10.1128/ec.4.12.2153-2159.2005.

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ABSTRACT The plasmodial surface anion channel (PSAC), a novel ion channel induced on human erythrocytes infected with Plasmodium falciparum, mediates increased permeability to nutrients and presumably supports intracellular parasite growth. Isotope flux studies indicate that other malaria parasites also increase the permeability of their host erythrocytes, but the precise mechanisms are unknown. Channels similar to PSAC or alternative mechanisms, such as the upregulation of endogenous host transporters, might fulfill parasite nutrient demands. Here we evaluated these possibilities with rhesus

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Sharp, Paul M., Lindsey J. Plenderleith, and Beatrice H. Hahn. "Ape Origins of Human Malaria." Annual Review of Microbiology 74, no. 1 (2020): 39–63. http://dx.doi.org/10.1146/annurev-micro-020518-115628.

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African apes harbor at least twelve Plasmodium species, some of which have been a source of human infection. It is now well established that Plasmodium falciparum emerged following the transmission of a gorilla parasite, perhaps within the last 10,000 years, while Plasmodium vivax emerged earlier from a parasite lineage that infected humans and apes in Africa before the Duffy-negative mutation eliminated the parasite from humans there. Compared to their ape relatives, both human parasites have greatly reduced genetic diversity and an excess of nonsynonymous mutations, consistent with severe ge

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Hang, Jing-Wen, Farhana Tukijan, Erica-Qian-Hui Lee, Shifana Raja Abdeen, Yaw Aniweh, and Benoit Malleret. "Zoonotic Malaria: Non-Laverania Plasmodium Biology and Invasion Mechanisms." Pathogens 10, no. 7 (2021): 889. http://dx.doi.org/10.3390/pathogens10070889.

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Malaria, which is caused by Plasmodium parasites through Anopheles mosquito transmission, remains one of the most life-threatening diseases affecting hundreds of millions of people worldwide every year. Plasmodium vivax, which accounts for the majority of cases of recurring malaria caused by the Plasmodium (non-Laverania) subgenus, is an ancient and continuing zoonosis originating from monkey hosts probably outside Africa. The emergence of other zoonotic malarias (P. knowlesi, P. cynomolgi, and P. simium) further highlights the seriousness of the disease. The severity of this epidemic disease

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Pegoraro, Mirko, and Gareth D. Weedall. "Malaria in the ‘Omics Era’." Genes 12, no. 6 (2021): 843. http://dx.doi.org/10.3390/genes12060843.

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Genomics has revolutionised the study of the biology of parasitic diseases. The first Eukaryotic parasite to have its genome sequenced was the malaria parasite Plasmodium falciparum. Since then, Plasmodium genomics has continued to lead the way in the study of the genome biology of parasites, both in breadth—the number of Plasmodium species’ genomes sequenced—and in depth—massive-scale genome re-sequencing of several key species. Here, we review some of the insights into the biology, evolution and population genetics of Plasmodium gained from genome sequencing, and look at potential new avenue

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Matz, Joachim M., Alyssa Ingmundson, Jean Costa Nunes, Werner Stenzel, Kai Matuschewski, and Taco W. A. Kooij. "In Vivo Function of PTEX88 in Malaria Parasite Sequestration and Virulence." Eukaryotic Cell 14, no. 6 (2015): 528–34. http://dx.doi.org/10.1128/ec.00276-14.

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ABSTRACT Malaria pathology is linked to remodeling of red blood cells by eukaryotic Plasmodium parasites. Central to host cell refurbishment is the trafficking of parasite-encoded virulence factors through the Plasmodium translocon of exported proteins (PTEX). Much of our understanding of its function is based on experimental work with cultured Plasmodium falciparum , yet direct consequences of PTEX impairment during an infection remain poorly defined. Using the murine malaria model parasite Plasmodium berghei , it is shown here that efficient sequestration to the pulmonary, adipose, and brain

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Saralamba, Sompob, Wirichada Pan-Ngum, Richard J. Maude, et al. "Intrahost modeling of artemisinin resistance in Plasmodium falciparum." Proceedings of the National Academy of Sciences 108, no. 1 (2010): 397–402. http://dx.doi.org/10.1073/pnas.1006113108.

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Artemisinin-resistant Plasmodium falciparum malaria has emerged in western Cambodia. Resistance is characterized by prolonged in vivo parasite clearance times (PCTs) following artesunate treatment. The biological basis is unclear. The hypothesis that delayed parasite clearance results from a stage-specific reduction in artemisinin sensitivity of the circulating young asexual parasite ring stages was examined. A mathematical model was developed, describing the intrahost parasite stage-specific pharmacokinetic–pharmacodynamic relationships. Model parameters were estimated using detailed pharmaco

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Sanyal, Sohini, Stéphane Egée, Guillaume Bouyer, et al. "Plasmodium falciparum STEVOR proteins impact erythrocyte mechanical properties." Blood 119, no. 2 (2012): e1-e8. http://dx.doi.org/10.1182/blood-2011-08-370734.

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Infection of erythrocytes with the human malaria parasite, Plasmodium falciparum, results in dramatic changes to the host cell structure and morphology. The predicted functional localization of the STEVOR proteins at the erythrocyte surface suggests that they may be involved in parasite-induced modifications of the erythrocyte membrane during parasite development. To address the biologic function of STEVOR proteins, we subjected a panel of stevor transgenic parasites and wild-type clonal lines exhibiting different expression levels for stevor genes to functional assays exploring parasite-induc

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Zohra, Aja Fatimah, Samsul Anwar, Aida Fitri, and Muhammad Haikal Nasution. "Klasifikasi Wilayah Provinsi Aceh Berdasarkan Tingkat Kerentanan Kasus Malaria Tahun 2015 – 2018." JURNAL KESEHATAN LINGKUNGAN INDONESIA 18, no. 1 (2019): 25. http://dx.doi.org/10.14710/jkli.18.1.25-33.

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Latar belakang: Malaria merupakan salah satu kasus penyakit yang tidak pernah hilang. World Health Organization (WHO) memperkirakan sebanyak 300 hingga 500 juta orang terinfeksi malaria tiap tahunnya dengan angka kematian berkisar antara 1,5 hingga 2,7 juta pertahun. Pemerintah melalui Rencana Pembangunan Jangka Menengah Nasional (RPJMN) tahun 2015-2019 menargetkan sebanyak 300 kabupaten/kota akan memiliki sertifikasi eliminasi malaria pada tahun 2019. Penelitian ini merupakan penelitian pendahuluan terkait dengan distribusi dan prevalensi kejadian malaria di Provinsi Aceh. Meskipun sebagian b

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Robinson, Ailie, Annette O. Busula, Mirjam A. Voets, et al. "Plasmodium-associated changes in human odor attract mosquitoes." Proceedings of the National Academy of Sciences 115, no. 18 (2018): E4209—E4218. http://dx.doi.org/10.1073/pnas.1721610115.

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Malaria parasites (Plasmodium) can change the attractiveness of their vertebrate hosts to Anopheles vectors, leading to a greater number of vector–host contacts and increased transmission. Indeed, naturally Plasmodium-infected children have been shown to attract more mosquitoes than parasite-free children. Here, we demonstrate Plasmodium-induced increases in the attractiveness of skin odor in Kenyan children and reveal quantitative differences in the production of specific odor components in infected vs. parasite-free individuals. We found the aldehydes heptanal, octanal, and nonanal to be pro

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Bruce, M. C., P. Alano, S. Duthie, and R. Carter. "Commitment of the malaria parasite Plasmodium falciparum to sexual and asexual development." Parasitology 100, no. 2 (1990): 191–200. http://dx.doi.org/10.1017/s0031182000061199.

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SUMMARYBlood-stage malaria parasites in the vertebrate host can develop either into the asexual, multiplying forms, called schizonts, or into gametocytes, the sexual stages of the parasite. In the present work we studied the differentiation into asexual parasites or gametocytes of the progeny of single, isolated schizonts of the clone 3D7A of Plasinodium falciparum, using monoclonal antibodies specific for the sexual or asexual stages of the parasite. We observed that schizonts obtained from a continuous culture undergoing serial cycles of growth and dilution with fresh red blood cells produce

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Ndung'u, Loise, Benard Langat, Esther Magiri, et al. "Amodiaquine resistance in Plasmodium berghei is associated with PbCRT His95Pro mutation, loss of chloroquine, artemisinin and primaquine sensitivity, and high transcript levels of key transporters." Wellcome Open Research 2 (June 20, 2017): 44. http://dx.doi.org/10.12688/wellcomeopenres.11768.1.

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Background: The human malaria parasite Plasmodium falciparum has evolved complex drug evasion mechanisms to all available antimalarials. To date, the combination of amodiaquine-artesunate is among the drug of choice for treatment of uncomplicated malaria. In this combination, a short acting, artesunate is partnered with long acting, amodiaquine for which resistance may emerge rapidly especially in high transmission settings. Here, we used a rodent malaria parasite Plasmodium berghei ANKA as a surrogate of P. falciparum to investigate the mechanisms of amodiaquine resistance. Methods: We used s

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Sultan, Ali A., Vandana Thathy, Victor Nussenzweig, and Robert Ménard. "Green Fluorescent Protein as a Marker in Plasmodium berghei Transformation." Infection and Immunity 67, no. 5 (1999): 2602–6. http://dx.doi.org/10.1128/iai.67.5.2602-2606.1999.

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ABSTRACT We present a new marker that confers both resistance to pyrimethamine and green fluorescent protein-based fluorescence on the malarial parasite Plasmodium berghei. A single copy of the cassette integrated into the genome is sufficient to direct fluorescence in parasites throughout the life cycle, in both its mosquito and vertebrate hosts. Erythrocyte stages of the parasite that express the marker can be sorted from control parasites by flow cytometry. Pyrimethamine pressure is not necessary for maintaining the cassette in transformed parasites during their sporogonic cycle in mosquito

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Dwithania, Mareza, Nuzulia Irawati, and Rosfita Rasyid. "Insiden Malaria di Puskesmas Sungai Durian dan Puskesmas Talawi Kota Sawahlunto Bulan Oktober 2011 sampai Februari 2012." Jurnal Kesehatan Andalas 2, no. 2 (2013): 76. http://dx.doi.org/10.25077/jka.v2i2.124.

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AbstrakMalaria masih merupakan masalah kesehatan dunia, termasuk Indonesia karena angka kesakitan dan kematian akibat penyakit ini cukup tinggi. Tingginya insiden malaria pada suatu daerah dapat dipengaruhi oleh parasit, hospes, dan vektor. Sawahlunto sebagai suatu daerah perbukitan memiliki risiko tinggi untuk penyebaran dan penularan penyakit malaria. Tujuan penelitian ini adalah untuk mengetahui insiden dan distribusi malaria menurut spesies parasit penyebab malaria, derajat infeksi berdasarkan hitung parasit, umur, dan jenis kelamin penderita. Penelitian ini dilakukan terhadap pasien denga

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Sanderson, Theo, and Julian C. Rayner. "PhenoPlasm: a database of disruption phenotypes for malaria parasite genes." Wellcome Open Research 2 (June 21, 2017): 45. http://dx.doi.org/10.12688/wellcomeopenres.11896.1.

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Two decades after the first Plasmodium transfection, attempts have been made to disrupt more than 3,151 genes in malaria parasites, across five Plasmodium species. While results from rodent malaria transfections have been curated and systematised, empowering large-scale analysis, phenotypic data from human malaria parasite transfections currently exists as individual reports scattered across a the literature. To facilitate systematic analysis of published experimental genetic data across Plasmodium species, we have built PhenoPlasm (http://www.phenoplasm.org), a database of phenotypes generate

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Sanderson, Theo, and Julian C. Rayner. "PhenoPlasm: a database of disruption phenotypes for malaria parasite genes." Wellcome Open Research 2 (July 24, 2017): 45. http://dx.doi.org/10.12688/wellcomeopenres.11896.2.

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Two decades after the first Plasmodium transfection, attempts have been made to disrupt more than 3,151 genes in malaria parasites, across five Plasmodium species. While results from rodent malaria transfections have been curated and systematised, empowering large-scale analysis, phenotypic data from human malaria parasite transfections currently exists as individual reports scattered across a the literature. To facilitate systematic analysis of published experimental genetic data across Plasmodium species, we have built PhenoPlasm (http://www.phenoplasm.org), a database of phenotypes generate

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Morgan, D. M. L., U. Bachrach, Y. G. Assaraf, E. Harari, and J. Golenser. "The effect of purified aminoaldehydes produced by polyamine oxidation on the development in vitro of Plasmodium falciparum in normal and glucose-6-phosphate-dehydrogenase-deficient erythrocytes." Biochemical Journal 236, no. 1 (1986): 97–101. http://dx.doi.org/10.1042/bj2360097.

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Purified aminoaldehydes produced by polyamine oxidation were toxic to the malarial parasite, Plasmodium falciparum, cultured in human erythrocytes. There was a profound effect on young ring forms, and, during maturation, parasites became more sensitive to the aldehydes. Oxidation of the aldehydes abolished the lethal effect. The plasmodia within glucose-6-phosphate-dehydrogenase (G6PD)-deficient erythrocytes were more sensitive to mono- and di-aldehydes than were parasites in normal erythrocytes. G6PD-deficient erythrocytes were also more sensitive to pretreatment with the dialdehyde produced

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VENTIM, RITA, JOANA MORAIS, SARA PARDAL, LUÍSA MENDES, JAIME A. RAMOS, and JAVIER PÉREZ-TRIS. "Host-parasite associations and host-specificity in haemoparasites of reed bed passerines." Parasitology 139, no. 3 (2012): 310–16. http://dx.doi.org/10.1017/s0031182011002083.

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SUMMARYThe host specificity and host sharing of avian haemoparasites (genera Haemoproteus and Plasmodium) is still poorly known, although they infect a large proportion of several studied bird populations. This study used molecular techniques to detect haemoparasites in marsh warblers and in other passerines that feed in reed beds, at 4 sites in Portugal. The host-specificity of the parasite lineages was analysed and compared with other cases described in the literature to assess whether apparent host specificity changes according to the studied system. Nine lineages of Haemoproteus and 15 of

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SOOMRO, FAROOQ RAHMAN, GHULAM MURTAZA PATHAN, and JUMA KHAN KAKAR. "MALARIAL PARASITE." Professional Medical Journal 16, no. 03 (2009): 377–79. http://dx.doi.org/10.29309/tpmj/2009.16.03.2798.

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Objectives: To determine the slide positivity rate and to document the different species of malarial parasite at district Shikarpur,Sindh, Pakistan. D e s i g n : A retrospective study. Setting: This study was conducted at district Malaria control centre Shikarur with collaborationof Pathology Department CMC Larkana and Leishmaniaisis/Mosquito Zoology Lab: University of Balochistan Quetta overthe period of one yeari.e. 2006. Patients a n d M e t h o d s : During the study period blood smears were prepared from the suspected cases of malaria. The patients withdifferentiated fever referred from

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Van Tyne, Daria, Alessandro D. Uboldi, Julie Healer, Alan F. Cowman, and Dyann F. Wirth. "Modulation of PF10_0355 (MSPDBL2) Alters Plasmodium falciparum Response to Antimalarial Drugs." Antimicrobial Agents and Chemotherapy 57, no. 7 (2013): 2937–41. http://dx.doi.org/10.1128/aac.02574-12.

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ABSTRACTMalaria's ability to rapidly adapt to new drugs has allowed it to remain one of the most devastating infectious diseases of humans. Understanding and tracking the genetic basis of these adaptations are critical to the success of treatment and intervention strategies. The novel antimalarial resistance locusPF10_0355(Pfmspdbl2) was previously associated with the parasite response to halofantrine, and functional validation confirmed that overexpression of this gene lowered parasite sensitivity to both halofantrine and the structurally related antimalarials mefloquine and lumefantrine, pre

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VALKIŪNAS, GEDIMINAS, MIKAS ILGŪNAS, DOVILĖ BUKAUSKAITĖ, VAIDAS PALINAUSKAS, RASA BERNOTIENĖ, and TATJANA A. IEZHOVA. "Molecular characterization and distribution of Plasmodium matutinum, a common avian malaria parasite." Parasitology 144, no. 13 (2017): 1726–35. http://dx.doi.org/10.1017/s0031182017000737.

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SUMMARYSpecies of Plasmodium (Plasmodiidae, Haemosporida) are widespread and cause malaria, which can be severe in avian hosts. Molecular markers are essential to detect and identify parasites, but still absent for many avian malaria and related haemosporidian species. Here, we provide first molecular characterization of Plasmodium matutinum, a common agent of avian malaria. This parasite was isolated from a naturally infected thrush nightingale Luscinia luscinia (Muscicapidae). Fragments of mitochondrial, apicoplast and nuclear genomes were obtained. Domestic canaries Serinus canaria were sus

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SIJBRANDA, D. C., B. D. GARTRELL, Z. L. GRANGE, and L. HOWE. "Use of a real-time PCR to explore the intensity of Plasmodium spp. infections in native, endemic and introduced New Zealand birds." Parasitology 144, no. 13 (2017): 1743–51. http://dx.doi.org/10.1017/s0031182017000919.

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SUMMARYAvian malaria, caused by Plasmodium spp., is an emerging disease in New Zealand (NZ). To detect Plasmodium spp. infection and quantify parasite load in NZ birds, a real-time polymerase chain reaction (PCR) (qPCR) protocol was used and compared with a nested PCR (nPCR) assay. A total of 202 blood samples from 14 bird species with known nPCR results were tested. The qPCR prevalences for introduced, native and endemic species groups were 70, 11 and 21%, respectively, with a sensitivity and specificity of 96·7 and 98%, respectively, for the qPCR, while a sensitivity and specificity of 80·9

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Guttery, David S., Abhinay Ramaprasad, David J. P. Ferguson, et al. "MRE11 Is Crucial for Malaria Parasite Transmission and Its Absence Affects Expression of Interconnected Networks of Key Genes Essential for Life." Cells 9, no. 12 (2020): 2590. http://dx.doi.org/10.3390/cells9122590.

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The meiotic recombination 11 protein (MRE11) plays a key role in DNA damage response and maintenance of genome stability. However, little is known about its function during development of the malaria parasite Plasmodium. Here, we present a functional, ultrastructural and transcriptomic analysis of Plasmodium parasites lacking MRE11 during its life cycle in both mammalian and mosquito vector hosts. Genetic disruption of Plasmodium berghei mre11 (PbMRE11) results in significant retardation of oocyst development in the mosquito midgut associated with cytoplasmic and nuclear degeneration, along wi

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Frame, I. J., Emilio F. Merino, Vern L. Schramm, María B. Cassera, and Myles H. Akabas. "Malaria parasite type 4 equilibrative nucleoside transporters (ENT4) are purine transporters with distinct substrate specificity." Biochemical Journal 446, no. 2 (2012): 179–90. http://dx.doi.org/10.1042/bj20112220.

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Malaria, caused by Plasmodia parasites, affects hundreds of millions of people. As purine auxotrophs, Plasmodia use transporters to import host purines for subsequent metabolism by the purine salvage pathway. Thus purine transporters are attractive drug targets. All sequenced Plasmodia genomes encode four ENTs (equilibrative nucleoside transporters). During the pathogenic intraerythrocytic stages, ENT1 is a major route of purine nucleoside/nucleobase transport. Another plasma membrane purine transporter exists because Plasmodium falciparum ENT1-knockout parasites survive at supraphysiological

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Wel, Anna M. van der, Ana M. Tomás, Clemens H. M. Kocken, et al. "Transfection of the Primate Malaria Parasite Plasmodium knowlesi Using Entirely Heterologous Constructs." Journal of Experimental Medicine 185, no. 8 (1997): 1499–504. http://dx.doi.org/10.1084/jem.185.8.1499.

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The recently developed transfection systems for Plasmodium berghei and Plasmodium falciparum offer important new tools enabling further insight into the biology of malaria parasites. These systems rely upon artificial parasite–host combinations which do not allow investigation into the complex interactions between parasites and their natural hosts. Here we report on stable transfection of Plasmodium knowlesi (a primate malaria parasite that clusters phylogenetically with P. vivax) for which both natural and artificial experimental hosts are available. Transfection of this parasite offers the o

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Hentzschel, Franziska, Klara Obrova, and Matthias Marti. "No evidence for Ago2 translocation from the host erythrocyte into the Plasmodium parasite." Wellcome Open Research 5 (May 12, 2020): 92. http://dx.doi.org/10.12688/wellcomeopenres.15852.1.

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Background: Plasmodium parasites rely on various host factors to grow and replicate within red blood cells (RBC). While many host proteins are known that mediate parasite adhesion and invasion, few examples of host enzymes co-opted by the parasite during intracellular development have been described. Recent studies suggested that the host protein Argonaute 2 (Ago2), which is involved in RNA interference, can translocate into the parasite and affect its development. Here, we investigated this hypothesis. Methods: We used several different monoclonal antibodies to test for Ago2 localisation in t

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Hentzschel, Franziska, Klara Obrova, and Matthias Marti. "No evidence for Ago2 translocation from the host erythrocyte into the Plasmodium parasite." Wellcome Open Research 5 (November 20, 2020): 92. http://dx.doi.org/10.12688/wellcomeopenres.15852.2.

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Background: Plasmodium parasites rely on various host factors to grow and replicate within red blood cells (RBC). While many host proteins are known that mediate parasite adhesion and invasion, few examples of host enzymes co-opted by the parasite during intracellular development have been described. Recent studies suggested that the host protein Argonaute 2 (Ago2), which is involved in RNA interference, can translocate into the parasite and affect its development. Here, we investigated this hypothesis. Methods: We used several different monoclonal antibodies to test for Ago2 localisation in t

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Pereira, Pedro H. Scarpelli, Chiara Curra, and Celia R. S. Garcia. "Ubiquitin Proteasome System as a Potential Drug Target for Malaria." Current Topics in Medicinal Chemistry 18, no. 5 (2018): 315–20. http://dx.doi.org/10.2174/1568026618666180427145308.

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Parasites of Plasmodium genus are responsible for causing malaria in humans. Resistant strains to all available antimalarials can be found in several locations around the globe, including parasites resistant to the latest generation of combination drugs, such as piperaquine + artemisinin. Plasmodium develops between two completely different hosts such as a vertebrate one and the mosquito vector, thus it has the ability to adapt to very extreme and different environments. Through the complex life cycle in the hosts, Plasmodium invades and replicates in totally different cells thus making the st

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De Nys, Hélène M., Sébastien Calvignac-Spencer, Ursula Thiesen, et al. "Age-related effects on malaria parasite infection in wild chimpanzees." Biology Letters 9, no. 4 (2013): 20121160. http://dx.doi.org/10.1098/rsbl.2012.1160.

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Wild great apes are widely infected with a number of malaria parasites ( Plasmodium spp.). Yet, nothing is known about the biology of these infections in the wild. Using faecal samples collected from wild chimpanzees, we investigated the effect of age on Plasmodium spp. detection rates. The data show a strong association between age and malaria parasite positivity, with significantly lower detection rates in adults. This suggests that, as in humans, individuals reaching adulthood have mounted an effective protective immunity against malaria parasites.

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Sá e Cunha, Cláudia, Britta Nyboer, Kirsten Heiss, et al. "Plasmodium berghei EXP-1 interacts with host Apolipoprotein H during Plasmodium liver-stage development." Proceedings of the National Academy of Sciences 114, no. 7 (2017): E1138—E1147. http://dx.doi.org/10.1073/pnas.1606419114.

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The first, obligatory replication phase of malaria parasite infections is characterized by rapid expansion and differentiation of single parasites in liver cells, resulting in the formation and release of thousands of invasive merozoites into the bloodstream. Hepatic Plasmodium development occurs inside a specialized membranous compartment termed the parasitophorous vacuole (PV). Here, we show that, during the parasite’s hepatic replication, the C-terminal region of the parasitic PV membrane protein exported protein 1 (EXP-1) binds to host Apolipoprotein H (ApoH) and that this molecular intera

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SILVA, JOANA C., AMY EGAN, ROBERT FRIEDMAN, JAMES B. MUNRO, JANE M. CARLTON, and AUSTIN L. HUGHES. "Genome sequences reveal divergence times of malaria parasite lineages." Parasitology 138, no. 13 (2010): 1737–49. http://dx.doi.org/10.1017/s0031182010001575.

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SUMMARYObjectiveThe evolutionary history of human malaria parasites (genus Plasmodium) has long been a subject of speculation and controversy. The complete genome sequences of the two most widespread human malaria parasites, P. falciparum and P. vivax, and of the monkey parasite P. knowlesi are now available, together with the draft genomes of the chimpanzee parasite P. reichenowi, three rodent parasites, P. yoelii yoelli, P. berghei and P. chabaudi chabaudi, and one avian parasite, P. gallinaceum.MethodsWe present here an analysis of 45 orthologous gene sequences across the eight species that

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MEDEIROS, MATTHEW C. I., ROBERT E. RICKLEFS, JEFFREY D. BRAWN, and GABRIEL L. HAMER. "Plasmodium prevalence across avian host species is positively associated with exposure to mosquito vectors." Parasitology 142, no. 13 (2015): 1612–20. http://dx.doi.org/10.1017/s0031182015001183.

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SUMMARYThe prevalence of vector-borne parasites varies greatly across host species, and this heterogeneity has been used to relate infectious disease susceptibility to host species traits. However, a few empirical studies have directly associated vector-borne parasite prevalence with exposure to vectors across hosts. Here, we use DNA sequencing of blood meals to estimate utilization of different avian host species by Culex mosquitoes, and relate utilization by these malaria vectors to avian Plasmodium prevalence. We found that avian host species that are highly utilized as hosts by avian malar

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Vigário, Ana Margarida, Elodie Belnoue, Ana Cumano та ін. "Inhibition of Plasmodium yoelii blood-stage malaria by interferon α through the inhibition of the production of its target cell, the reticulocyte". Blood 97, № 12 (2001): 3966–71. http://dx.doi.org/10.1182/blood.v97.12.3966.

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The effect of a recombinant hybrid human interferon α (IFN-α) (which cross-reacts with murine cells) on C57BL/6 mice infected with Plasmodium yoelii sporozoites or parasitized erythrocytes was determined. IFN-α did not inhibit the development of the parasite in the liver, but it did reduce the blood parasite load and the hepatosplenomegaly induced by the infection in mice injected with blood-stage parasites. The extent of anemia in IFN-α–treated and control mice was similar, despite the lower parasite load in the IFN-α–treated mice. The reduced blood parasite load in IFN-α–treated mice was ass

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Ndung'u, Loise, Benard Langat, Esther Magiri, et al. "Amodiaquine resistance in Plasmodium berghei is associated with PbCRT His95Pro mutation, loss of chloroquine, artemisinin and primaquine sensitivity, and high transcript levels of key transporters." Wellcome Open Research 2 (June 6, 2018): 44. http://dx.doi.org/10.12688/wellcomeopenres.11768.2.

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Background: The human malaria parasite Plasmodium falciparum has evolved drug evasion mechanisms to all available antimalarials. The combination of amodiaquine-artesunate is among the drug of choice for treatment of uncomplicated malaria. In this combination, a short-acting, artesunate is partnered with long-acting, amodiaquine for which resistance may emerge rapidly especially in high transmission settings. Here, we used a rodent malaria parasite Plasmodium berghei ANKA as a surrogate of P. falciparum to investigate the mechanisms of amodiaquine resistance. Methods: We used the ramp up approa

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Fonager, Jannik, Erica M. Pasini, Joanna A. M. Braks, et al. "Reduced CD36-dependent tissue sequestration of Plasmodium-infected erythrocytes is detrimental to malaria parasite growth in vivo." Journal of Experimental Medicine 209, no. 1 (2011): 93–107. http://dx.doi.org/10.1084/jem.20110762.

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Adherence of parasite-infected red blood cells (irbc) to the vascular endothelium of organs plays a key role in the pathogenesis of Plasmodium falciparum malaria. The prevailing hypothesis of why irbc adhere and sequester in tissues is that this acts as a mechanism of avoiding spleen-mediated clearance. Irbc of the rodent parasite Plasmodium berghei ANKA sequester in a fashion analogous to P. falciparum by adhering to the host receptor CD36. To experimentally determine the significance of sequestration for parasite growth, we generated a mutant P. berghei ANKA parasite with a reduced CD36-medi

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Monteiro, Eliana Ferreira, Carmen Fernandez-Becerra, Maisa da Silva Araujo, et al. "Naturally Acquired Humoral Immunity against Malaria Parasites in Non-Human Primates from the Brazilian Amazon, Cerrado and Atlantic Forest." Pathogens 9, no. 7 (2020): 525. http://dx.doi.org/10.3390/pathogens9070525.

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Non-human primates (NHPs) have been shown to be infected by parasites of the genus Plasmodium, the etiological agent of malaria in humans, creating potential risks of zoonotic transmission. Plasmodium brasilianum, a parasite species similar to P. malariae of humans, have been described in NHPs from Central and South America, including Brazil. The merozoite surface protein 1 (MSP1), besides being a malaria vaccine candidate, is highly immunogenic. Due to such properties, we tested this protein for the diagnosis of parasite infection. We used recombinant proteins of P. malariae MSP1, as well as

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