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1

Severins, Maite, Don Klinkenberg, and Hans Heesterbeek. "How selection forces dictate the variant surface antigens used by malaria parasites." Journal of The Royal Society Interface 9, no. 67 (2011): 246–60. http://dx.doi.org/10.1098/rsif.2011.0239.

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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 mea
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2

Forbes, Mark R., André Morrill, and Jennifer Schellinck. "Host species exploitation and discrimination by animal parasites." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1719 (2017): 20160090. http://dx.doi.org/10.1098/rstb.2016.0090.

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Parasite species often show differential fitness on different host species. We developed an equation-based model to explore conditions favouring host species exploitation and discrimination. In our model, diploid infective stages randomly encountered hosts of two species; the parasite's relative fitness in exploiting each host species, and its ability to discriminate between them, was determined by the parasite's genotype at two independent diallelic loci. Relative host species frequency determined allele frequencies at the exploitation locus, whereas differential fitness and combined host den
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3

Opperdoes, Fred R. "Subcellular biochemistry (intracellular parasites, vol 18." Transactions of the Royal Society of Tropical Medicine and Hygiene 88, no. 3 (1994): 368. http://dx.doi.org/10.1016/0035-9203(94)90133-3.

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4

Hanssen, Sveinn Are, Christian Sonne, Jan Ove Bustnes, et al. "Anti-parasite treatment and blood biochemistry in raptor nestlings." Canadian Journal of Zoology 95, no. 9 (2017): 685–93. http://dx.doi.org/10.1139/cjz-2016-0040.

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We investigated the effects of parasite removal on various blood clinical–chemical variables (BCCVs). BCCVs are indicators of health, reflecting, e.g., homeostasis of liver, kidney function, and bone metabolism. The study was conducted in Norway on chicks of two predatory birds: White-tailed Eagle (Haliaeetus albicilla (L., 1758)) and Northern Goshawk (Accipiter gentilis (L., 1758)). Chicks were treated against both endoparasites (internal parasites) and ectoparasites (external parasites). We treated against ectoparasites by spraying nests with pyrethrins. Within nests, chicks were randomly tr
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5

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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6

Langford, C. K., R. J. S. Burchmore, D. T. Hart, W. Wagner, and S. M. Landfear. "Biochemistry and molecular genetics of Leishmania glucose transporters." Parasitology 108, S1 (1994): S73—S83. http://dx.doi.org/10.1017/s0031182000075740.

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SUMMARYGlucose is utilized as a significant source of metabolic energy by Leishmania parasites. This sugar is accumulated by the parasite via a specific carrier-mediated transport system located in the parasite membrane. Parasites may also contain another transporter that shuttles glucose between the cytoplasm and the glycosome, a membrane-bound organelle where the early steps of glycolysis occur. The transport systems of both the insect stage promastigotes and the intracellular amastigotes have been characterized and shown to have kinetic properties that are consistent with the different phys
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7

HENRY, CELIA. "Drug researchers target biochemistry of malaria parasites." Chemical & Engineering News 77, no. 36 (1999): 9. http://dx.doi.org/10.1021/cen-v077n036.p009.

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8

Prior, Kimberley F., Benita Middleton, Alíz T. Y. Owolabi, et al. "Synchrony between daily rhythms of malaria parasites and hosts is driven by an essential amino acid." Wellcome Open Research 6 (July 22, 2021): 186. http://dx.doi.org/10.12688/wellcomeopenres.16894.1.

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Background: Rapid asexual replication of blood stage malaria parasites is responsible for the severity of disease symptoms and fuels the production of transmission forms. Here, we demonstrate that the Plasmodium chabaudi’s schedule for asexual replication can be orchestrated by isoleucine, a metabolite provided to the parasite in periodic manner due to the host’s rhythmic intake of food. Methods: We infect female C57BL/6 and Per1/2-null TTFL clock-disrupted mice with 1×105 red blood cells containing P. chabaudi (DK genotype). We perturb the timing of rhythms in asexual replication and host fee
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9

Duneau, David, and Dieter Ebert. "The role of moulting in parasite defence." Proceedings of the Royal Society B: Biological Sciences 279, no. 1740 (2012): 3049–54. http://dx.doi.org/10.1098/rspb.2012.0407.

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Parasitic infections consist of a succession of steps during which hosts and parasites interact in specific manners. At each step, hosts can use diverse defence mechanisms to counteract the parasite's attempts to invade and exploit them. Of these steps, the penetration of parasites into the host is a key step for a successful infection and the epithelium is the first line of host defence. The shedding of this protective layer (moulting) is a crucial feature in the life cycle of several invertebrate and vertebrate taxa, and is generally considered to make hosts vulnerable to parasites and preda
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10

Kim, Ju Yeong, Myung-Hee Yi, and Tai-Soon Yong. "Allergen-like Molecules from Parasites." Current Protein & Peptide Science 21, no. 2 (2020): 186–202. http://dx.doi.org/10.2174/1389203720666190708154300.

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Parasite infections modulate immunologic responses, and the loss of parasite infections in the last two to three decades might explain the increased prevalence of allergic diseases in developed countries. However, parasites can enhance allergic responses. Parasites contain or release allergen-like molecules that induce the specific immunoglobulin, IgE, and trigger type-2 immune responses. Some parasites and their proteins, such as Anisakis and Echinococcus granulosus allergens, act as typical allergens. A number of IgE-binding proteins of various helminthic parasites are cross-reactive to othe
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11

Grüter, Christoph, Evelien Jongepier, and Susanne Foitzik. "Insect societies fight back: the evolution of defensive traits against social parasites." Philosophical Transactions of the Royal Society B: Biological Sciences 373, no. 1751 (2018): 20170200. http://dx.doi.org/10.1098/rstb.2017.0200.

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Insect societies face many social parasites that exploit their altruistic behaviours or their resources. Due to the fitness costs these social parasites incur, hosts have evolved various behavioural, chemical, architectural and morphological defence traits. Similar to bacteria infecting multicellular hosts, social parasites have to successfully go through several steps to exploit their hosts. Here, we review how social insects try to interrupt this sequence of events. They can avoid parasite contact by choosing to nest in parasite-free locales or evade attacks by adapting their colony structur
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12

Lester, R. J. G., and R. McVinish. "Does moving up a food chain increase aggregation in parasites?" Journal of The Royal Society Interface 13, no. 118 (2016): 20160102. http://dx.doi.org/10.1098/rsif.2016.0102.

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General laws in ecological parasitology are scarce. Here, we evaluate data on numbers of fish parasites published by over 200 authors to determine whether acquiring parasites via prey is associated with an increase in parasite aggregation. Parasite species were grouped taxonomically to produce 20 or more data points per group as far as possible. Most parasites that remained at one trophic level were less aggregated than those that had passed up a food chain. We use a stochastic model to show that high parasite aggregation in predators can be solely the result of the accumulation of parasites i
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13

Heinze, Jürgen. "The Origin of Workerless Parasites inLeptothorax(S. Str.) (Hymenoptera: Formicidae)." Psyche: A Journal of Entomology 102, no. 3-4 (1995): 195–214. http://dx.doi.org/10.1155/1995/69812.

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The evolutionary origin of workerless parasitic ants parasitizing colonies ofLeptothorax(s.str.) is investigated using data on morphology, chromosome number, and allozyme phenotype of both social parasites and their hosts. Of the three previously proposed pathways, the evolution of workerless parasites from guest ants or slave-makers is unlikely, at least according to a phenogram obtained by UPGMA clustering of Nei's similarities based on seven enzymes, lntraspecific evolution of the workerless parasitesDoronomyrmex goesswaldi, D. kutteri, andD. pacisfrom their common host,Leptothorax acervoru
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14

Al-Anouti, Fatme, Stanislas Tomavo, Stephen Parmley, and Sirinart Ananvoranich. "The Expression of Lactate Dehydrogenase Is Important for the Cell Cycle ofToxoplasma gondii." Journal of Biological Chemistry 279, no. 50 (2004): 52300–52311. http://dx.doi.org/10.1074/jbc.m409175200.

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InToxoplasma gondii, lactate dehydrogenase is encoded by two independent and developmentally regulated genesLDH1andLDH2. These genes and their products have been implicated in the control of a metabolic flux during parasite differentiation. To investigate the significance ofLDH1andLDH2in this process, we generated stable transgenic parasite lines in which the expression of these two expressed isoforms of lactate dehydrogenase was knocked down in a stage-specific manner. TheseLDHknockdown parasites exhibited variable growth rates in either the tachyzoite or the bradyzoite stage, as compared wit
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15

Mitchell, GH, TJ Hadley, MH McGinniss, FW Klotz, and LH Miller. "Invasion of erythrocytes by Plasmodium falciparum malaria parasites: evidence for receptor heterogeneity and two receptors." Blood 67, no. 5 (1986): 1519–21. http://dx.doi.org/10.1182/blood.v67.5.1519.1519.

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Abstract Plasmodium falciparum malaria parasites with different capabilities of invading sialic acid-deficient erythrocytes were identified. Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase-treated and Tn erythrocytes twice as efficiently as Thai-2 parasites cultured in normal erythrocytes and seven to ten times more efficiently than a cloned line of Camp parasites cultured in normal erythrocytes. All three parasite lines required sialic acid for optimal invasion, but Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase- treated erythrocytes with 45% efficiency
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16

Mitchell, GH, TJ Hadley, MH McGinniss, FW Klotz, and LH Miller. "Invasion of erythrocytes by Plasmodium falciparum malaria parasites: evidence for receptor heterogeneity and two receptors." Blood 67, no. 5 (1986): 1519–21. http://dx.doi.org/10.1182/blood.v67.5.1519.bloodjournal6751519.

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Plasmodium falciparum malaria parasites with different capabilities of invading sialic acid-deficient erythrocytes were identified. Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase-treated and Tn erythrocytes twice as efficiently as Thai-2 parasites cultured in normal erythrocytes and seven to ten times more efficiently than a cloned line of Camp parasites cultured in normal erythrocytes. All three parasite lines required sialic acid for optimal invasion, but Thai-2 parasites cultured in Tn erythrocytes invaded neuraminidase- treated erythrocytes with 45% efficiency whereas C
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17

Lafferty, Kevin D. "Biodiversity loss decreases parasite diversity: theory and patterns." Philosophical Transactions of the Royal Society B: Biological Sciences 367, no. 1604 (2012): 2814–27. http://dx.doi.org/10.1098/rstb.2012.0110.

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Past models have suggested host–parasite coextinction could lead to linear, or concave down relationships between free-living species richness and parasite richness. I explored several models for the relationship between parasite richness and biodiversity loss. Life cycle complexity, low generality of parasites and sensitivity of hosts reduced the robustness of parasite species to the loss of free-living species diversity. Food-web complexity and the ordering of extinctions altered these relationships in unpredictable ways. Each disassembly of a food web resulted in a unique relationship betwe
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18

Coetzer, Theresa L., and Dewaldt Engelbrecht. "To Each His Own: Fever Induces Different Suicide Mechanisms in Early and Late Stage Plasmodium falciparum Malaria Parasites in vitro." Blood 122, no. 21 (2013): 3427. http://dx.doi.org/10.1182/blood.v122.21.3427.3427.

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Abstract Malaria is characterised by cyclical febrile episodes that result from the rupture of mature schizont-infected erythrocytes releasing merozoites. In patients infected with Plasmodium falciparum, fever may reach peak temperatures as high as 41°C, last for 2-6 hours and recur every 48 hours, in accordance with the parasite life cycle. Febrile episodes typically have a deleterious effect on parasites, and probably benefit the host by aiding parasite clearance; however, a reduction in parasitemia may also be an advantage for the parasite by limiting the burden of infection on the host and
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19

Piña-Vázquez, Carolina, Magda Reyes-López, Guillermo Ortíz-Estrada, Mireya de la Garza, and Jesús Serrano-Luna. "Host-Parasite Interaction: Parasite-Derived and -Induced Proteases That Degrade Human Extracellular Matrix." Journal of Parasitology Research 2012 (2012): 1–24. http://dx.doi.org/10.1155/2012/748206.

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Parasitic protozoa are among the most important pathogens worldwide. Diseases such as malaria, leishmaniasis, amoebiasis, giardiasis, trichomoniasis, and trypanosomiasis affect millions of people. Humans are constantly threatened by infections caused by these pathogens. Parasites engage a plethora of surface and secreted molecules to attach to and enter mammalian cells. The secretion of lytic enzymes by parasites into host organs mediates critical interactions because of the invasion and destruction of interstitial tissues, enabling parasite migration to other sites within the hosts. Extracell
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20

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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21

Nagel, RL, and EF Jr Roth. "Malaria and red cell genetic defects." Blood 74, no. 4 (1989): 1213–21. http://dx.doi.org/10.1182/blood.v74.4.1213.1213.

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Abstract The study of inherited RBC resistance to malaria has increased our knowledge of the biochemistry and physiology of the host-parasite interaction and suggested potential sites for therapeutic intervention. Discovery by Jensen and Trager of the in vitro culture system for P falciparum has facilitated research in this area. Known RBC defects may affect invasion, growth, or merozoite liberation (Fig 1). Significant advances made in understanding mechanisms underlying protection against malaria should not obscure the fact that the data are far from complete. More knowledge is needed about
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22

Nagel, RL, and EF Jr Roth. "Malaria and red cell genetic defects." Blood 74, no. 4 (1989): 1213–21. http://dx.doi.org/10.1182/blood.v74.4.1213.bloodjournal7441213.

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The study of inherited RBC resistance to malaria has increased our knowledge of the biochemistry and physiology of the host-parasite interaction and suggested potential sites for therapeutic intervention. Discovery by Jensen and Trager of the in vitro culture system for P falciparum has facilitated research in this area. Known RBC defects may affect invasion, growth, or merozoite liberation (Fig 1). Significant advances made in understanding mechanisms underlying protection against malaria should not obscure the fact that the data are far from complete. More knowledge is needed about the influ
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23

Ezenwa, Vanessa O., Elizabeth A. Archie, Meggan E. Craft, et al. "Host behaviour–parasite feedback: an essential link between animal behaviour and disease ecology." Proceedings of the Royal Society B: Biological Sciences 283, no. 1828 (2016): 20153078. http://dx.doi.org/10.1098/rspb.2015.3078.

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Animal behaviour and the ecology and evolution of parasites are inextricably linked. For this reason, animal behaviourists and disease ecologists have been interested in the intersection of their respective fields for decades. Despite this interest, most research at the behaviour–disease interface focuses either on how host behaviour affects parasites or how parasites affect behaviour, with little overlap between the two. Yet, the majority of interactions between hosts and parasites are probably reciprocal, such that host behaviour feeds back on parasites and vice versa. Explicitly considering
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24

Diouani, Mohamed Fethi, Oussama Ouerghi, Kamel Belgacem, Maher Sayhi, Radu Ionescu, and Dhafer Laouini. "Casein-Conjugated Gold Nanoparticles for Amperometric Detection of Leishmania infantum." Biosensors 9, no. 2 (2019): 68. http://dx.doi.org/10.3390/bios9020068.

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Sensitive and reliable approaches targeting the detection of Leishmania are critical for effective early diagnosis and treatment of leishmaniasis. In this frame, this paper describes a rapid quantification assay to detect Leishmania parasites based on the combination of the electrocatalytic ability of gold nanoparticles (AuNPs) to act as a catalyst for the hydrogen formation reaction along with the specificity of the interaction between casein and the major surface protease of the Leishmania parasite, GP63. First, pure and casein-modified AuNPs were prepared and characterized by scanning elect
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25

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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26

Guilhem, Rascalou, Andrea Šimková, Serge Morand, and Sébastien Gourbière. "Within-host competition and diversification of macro-parasites." Journal of The Royal Society Interface 9, no. 76 (2012): 2936–46. http://dx.doi.org/10.1098/rsif.2012.0358.

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Although competitive speciation is more and more regarded as a plausible mechanism for sympatric speciation of non-parasite species, virtually no empirical or theoretical study has considered this evolutionary process to explain intra-host diversification of parasites. We expanded the theory of competitive speciation to parasite species looking at the effect of macro-parasite life history on the conditions for sympatric speciation under the so-called pleiotropic scenario. We included within-host competition in the classical Anderson and May framework assuming that individuals exploit within-ho
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27

Baker, F. G. W. "Parasites?" BioEssays 3, no. 3 (1985): 99. http://dx.doi.org/10.1002/bies.950030302.

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28

Bashey, Farrah. "Within-host competitive interactions as a mechanism for the maintenance of parasite diversity." Philosophical Transactions of the Royal Society B: Biological Sciences 370, no. 1675 (2015): 20140301. http://dx.doi.org/10.1098/rstb.2014.0301.

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Variation among parasite strains can affect the progression of disease or the effectiveness of treatment. What maintains parasite diversity? Here I argue that competition among parasites within the host is a major cause of variation among parasites. The competitive environment within the host can vary depending on the parasite genotypes present. For example, parasite strategies that target specific competitors, such as bacteriocins, are dependent on the presence and susceptibility of those competitors for success. Accordingly, which parasite traits are favoured by within-host selection can var
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29

O'Donnell, Aidan J., Kimberley F. Prior, and Sarah E. Reece. "Host circadian clocks do not set the schedule for the within-host replication of malaria parasites." Proceedings of the Royal Society B: Biological Sciences 287, no. 1932 (2020): 20200347. http://dx.doi.org/10.1098/rspb.2020.0347.

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Circadian clocks coordinate organisms' activities with daily cycles in their environment. Parasites are subject to daily rhythms in the within-host environment, resulting from clock-control of host activities, including immune responses. Parasites also exhibit rhythms in their activities: the timing of within-host replication by malaria parasites is coordinated to host feeding rhythms. Precisely which host feeding-related rhythm(s) parasites align with and how this is achieved are unknown. Understanding rhythmic replication in malaria parasites matters because it underpins disease symptoms and
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30

Xu, Shanghua, Shumiao Zhang, Xiaolong Hu, et al. "Temporal and spatial dynamics of gastrointestinal parasite infection in Père David’s deer." PeerJ 9 (May 5, 2021): e11335. http://dx.doi.org/10.7717/peerj.11335.

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Background The Père David’s deer (Elaphurus davidianus) population was established from only a small number of individuals. Their genetic diversity is therefore relatively low and transmissible (parasitic) diseases affecting them merit further attention. Parasitic infections can affect the health, survival, and population development of the host. However, few reports have been published on the gastrointestinal parasites of Père David’s deer. The aims of this study were: (1) to identify the intestinal parasites groups in Père David’s deer; (2) to determine their prevalence and burden and clarif
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31

Lytton, SD, B. Mester, J. Libman, A. Shanzer, and ZI Cabantchik. "Mode of action of iron (III) chelators as antimalarials: II. Evidence for differential effects on parasite iron-dependent nucleic acid synthesis." Blood 84, no. 3 (1994): 910–15. http://dx.doi.org/10.1182/blood.v84.3.910.910.

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Abstract Iron chelation treatment of red blood cells infected with Plasmodium falciparum selectively intervenes with iron-dependent metabolism of malaria parasites and inhibits their development. Highly permeant hydroxamate iron chelator RSFileum2 affects all parasite stages when cultures are continuously exposed to drug, but affects primarily ring stages when assessed for irreversible effects, ie, sustained inhibition remaining after drug removal. On the other hand, the hydrophilic and poorly permeant desferrioxamine (DFO) affects primarily trophozoite/schizont stages when tested either in th
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Lytton, SD, B. Mester, J. Libman, A. Shanzer, and ZI Cabantchik. "Mode of action of iron (III) chelators as antimalarials: II. Evidence for differential effects on parasite iron-dependent nucleic acid synthesis." Blood 84, no. 3 (1994): 910–15. http://dx.doi.org/10.1182/blood.v84.3.910.bloodjournal843910.

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Iron chelation treatment of red blood cells infected with Plasmodium falciparum selectively intervenes with iron-dependent metabolism of malaria parasites and inhibits their development. Highly permeant hydroxamate iron chelator RSFileum2 affects all parasite stages when cultures are continuously exposed to drug, but affects primarily ring stages when assessed for irreversible effects, ie, sustained inhibition remaining after drug removal. On the other hand, the hydrophilic and poorly permeant desferrioxamine (DFO) affects primarily trophozoite/schizont stages when tested either in the continu
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33

Huang, Xi. "Assessment of Associations between Malaria Parasites and Avian Hosts—A Combination of Classic System and Modern Molecular Approach." Biology 10, no. 7 (2021): 636. http://dx.doi.org/10.3390/biology10070636.

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Avian malaria and related haemosporidian parasites are responsible for fitness loss and mortality in susceptible bird species. This group of globally distributed parasites has long been used as a classical system for investigating host–parasite associations. The association between a parasite and its hosts can be assessed by the prevalence in the host population and infection intensity in a host individual, which, respectively, reflect the ability of the parasite to infect the host and reproduce within the host. However, the latter has long been poorly investigated due to numerous challenges,
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34

Suhonen, Jukka, Jaakko J. Ilvonen, Tommi Nyman, and Jouni Sorvari. "Brood parasitism in eusocial insects (Hymenoptera): role of host geographical range size and phylogeny." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1769 (2019): 20180203. http://dx.doi.org/10.1098/rstb.2018.0203.

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Interspecific brood parasitism is common in many animal systems. Brood parasites enter the nests of other species and divert host resources for producing their own offspring, which can lead to strong antagonistic parasite–host coevolution. Here, we look at commonalities among social insect species that are victims of brood parasites, and use phylogenetic data and information on geographical range size to predict which species are most probably to fall victims to brood parasites in the future. In our analyses, we focus on three eusocial hymenopteran groups and their brood parasites: (i) bumbleb
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35

Tubman, Venee N., Pedro Mejia, Boris E. Shmukler, et al. "Senicapoc, a Gardos Channel Inhibitor Developed to Treat Sickle Cell Disease, Exhibits Antimalarial Activity." Blood 124, no. 21 (2014): 743. http://dx.doi.org/10.1182/blood.v124.21.743.743.

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Abstract BACKGROUND: The inhibitor of the erythrocyte Gardos channel (KCNN-4, IK-1), senicapoc, was developed for treatment of sickle cell disease. Activation of the Gardos channel constitutes a major potassium leak pathway contributing to cellular dehydration. Administration of senicapoc to patients with sickle cell disease was well tolerated and reduced hemolysis through attenuation of sickle red cell dehydration, but failed to reduce the frequency of vaso-occlusive pain crises (Ataga KI et al. Br J Haematol 2011;153:92-104). Red cell volume regulation is critical both to the pathology of si
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36

Tadiri, Christina P., Marilyn E. Scott, and Gregor F. Fussmann. "Microparasite dispersal in metapopulations: a boon or bane to the host population?" Proceedings of the Royal Society B: Biological Sciences 285, no. 1885 (2018): 20181519. http://dx.doi.org/10.1098/rspb.2018.1519.

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Although connectivity can promote host species persistence in a metapopulation, dispersal may also enable disease transmission, an effect further complicated by the impact that parasite distribution may have on host–parasite population dynamics. We investigated the effects of connectivity and initial parasite distribution (clustered or dispersed) on microparasite–host dynamics in experimental metapopulations, using guppies and Gyrodactylus turnbulli . We created metapopulations of guppies divided into four subpopulations and introduced either a low level of parasites to all subpopulations (dis
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37

Carlson, Colin J., Tad A. Dallas, Laura W. Alexander, Alexandra L. Phelan, and Anna J. Phillips. "What would it take to describe the global diversity of parasites?" Proceedings of the Royal Society B: Biological Sciences 287, no. 1939 (2020): 20201841. http://dx.doi.org/10.1098/rspb.2020.1841.

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How many parasites are there on Earth? Here, we use helminth parasites to highlight how little is known about parasite diversity, and how insufficient our current approach will be to describe the full scope of life on Earth. Using the largest database of host–parasite associations and one of the world’s largest parasite collections, we estimate a global total of roughly 100 000–350 000 species of helminth endoparasites of vertebrates, of which 85–95% are unknown to science. The parasites of amphibians and reptiles remain the most poorly described, but the majority of undescribed species are pr
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38

Ginger, Michael L. "Niche metabolism in parasitic protozoa." Philosophical Transactions of the Royal Society B: Biological Sciences 361, no. 1465 (2005): 101–18. http://dx.doi.org/10.1098/rstb.2005.1756.

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Complete or partial genome sequences have recently become available for several medically and evolutionarily important parasitic protozoa. Through the application of bioinformatics complete metabolic repertoires for these parasites can be predicted. For experimentally intractable parasites insight provided by metabolic maps generated in silico has been startling. At its more extreme end, such bioinformatics reckoning facilitated the discovery in some parasites of mitochondria remodelled beyond previous recognition, and the identification of a non-photosynthetic chloroplast relic in malarial pa
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39

Angus, Brian J., Kesinee Chotivanich, Rachanee Udomsangpetch, and Nicholas J. White. "In Vivo Removal of Malaria Parasites From Red Blood Cells Without Their Destruction in Acute Falciparum Malaria." Blood 90, no. 5 (1997): 2037–40. http://dx.doi.org/10.1182/blood.v90.5.2037.

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Abstract During acute falciparum malaria infection, red blood cells (RBC) containing abundant ring-infected erythrocyte surface antigen (Pf 155 or RESA), but no intracellular parasites, are present in the circulation. These RESA-positive parasite negative RBC are not seen in parasite cultures in vitro. This indicates that in acute falciparum malaria there is active removal of intraerythrocytic parasites by a host mechanism in vivo (probably the spleen) without destruction of the parasitized RBC. This may explain the observed disparity between the drop in hematocrit and decrease in parasite cou
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40

Ezenwa, Vanessa O., and Matthew H. Snider. "Reciprocal relationships between behaviour and parasites suggest that negative feedback may drive flexibility in male reproductive behaviour." Proceedings of the Royal Society B: Biological Sciences 283, no. 1831 (2016): 20160423. http://dx.doi.org/10.1098/rspb.2016.0423.

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Parasites are ubiquitous components of the environment that contribute to behavioural and life-history variation among hosts. Although it is well known that host behaviour can affect parasite infection risk and that parasites can alter host behaviour, the potential for dynamic feedback between these processes is poorly characterized. Using Grant's gazelle ( Nanger granti ) as a model, we tested for reciprocal effects of behaviour on parasites and parasites on behaviour to understand whether behaviour–parasite feedback could play a role in maintaining variation in male reproductive behaviour. A
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41

Auld, Stuart K. J. R., Shona K. Tinkler, and Matthew C. Tinsley. "Sex as a strategy against rapidly evolving parasites." Proceedings of the Royal Society B: Biological Sciences 283, no. 1845 (2016): 20162226. http://dx.doi.org/10.1098/rspb.2016.2226.

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Why is sex ubiquitous when asexual reproduction is much less costly? Sex disrupts coadapted gene complexes; it also causes costs associated with mate finding and the production of males who do not themselves bear offspring. Theory predicts parasites select for host sex, because genetically variable offspring can escape infection from parasites adapted to infect the previous generations. We examine this using a facultative sexual crustacean, Daphnia magna, and its sterilizing bacterial parasite, Pasteuria ramosa . We obtained sexually and asexually produced offspring from wild-caught hosts and
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42

Maciej-Hulme, Marissa L., Mark A. Skidmore, and Helen P. Price. "The role of heparan sulfate in host macrophage infection by Leishmania species." Biochemical Society Transactions 46, no. 4 (2018): 789–96. http://dx.doi.org/10.1042/bst20170398.

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The leishmaniases are a group of neglected tropical diseases caused by parasites from the Leishmania genus. More than 20 Leishmania species are responsible for human disease, causing a broad spectrum of symptoms ranging from cutaneous lesions to a fatal visceral infection. There is no single safe and effective approach to treat these diseases and resistance to current anti-leishmanial drugs is emerging. New drug targets need to be identified and validated to generate novel treatments. Host heparan sulfates (HSs) are abundant, heterogeneous polysaccharides displayed on proteoglycans that bind v
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43

Cotter, S. C., D. Pincheira-Donoso, and R. Thorogood. "Defences against brood parasites from a social immunity perspective." Philosophical Transactions of the Royal Society B: Biological Sciences 374, no. 1769 (2019): 20180207. http://dx.doi.org/10.1098/rstb.2018.0207.

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Parasitic interactions are so ubiquitous that all multicellular organisms have evolved a system of defences to reduce their costs, whether the parasites they encounter are the classic parasites which feed on the individual, or brood parasites which usurp parental care. Many parallels have been drawn between defences deployed against both types of parasite, but typically, while defences against classic parasites have been selected to protect survival, those against brood parasites have been selected to protect the parent's inclusive fitness, suggesting that the selection pressures they impose a
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44

Magowan, C., RL Coppel, AO Lau, MM Moronne, G. Tchernia, and N. Mohandas. "Role of the Plasmodium falciparum mature-parasite-infected erythrocyte surface antigen (MESA/PfEMP-2) in malarial infection of erythrocytes." Blood 86, no. 8 (1995): 3196–204. http://dx.doi.org/10.1182/blood.v86.8.3196.3196.

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Abstract During intraerythrocytic growth of Plasmodium falciparum, several parasite proteins are transported from the parasite to the erythrocyte membrane, where they bind to membrane skeletal proteins. Mature-parasite-infected erythrocyte surface antigen (MESA) has previously been shown to associate with host erythrocyte membrane skeletal protein 4.1. Using a spontaneous mutant of P falciparum that has lost the ability to synthesize MESA and 4.1-deficient erythrocytes, we examined growth of MESA(+) and MESA(-) parasites in normal and 4.1-deficient erythrocytes. Viability of MESA(+) parasites
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45

Magowan, C., RL Coppel, AO Lau, MM Moronne, G. Tchernia, and N. Mohandas. "Role of the Plasmodium falciparum mature-parasite-infected erythrocyte surface antigen (MESA/PfEMP-2) in malarial infection of erythrocytes." Blood 86, no. 8 (1995): 3196–204. http://dx.doi.org/10.1182/blood.v86.8.3196.bloodjournal8683196.

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During intraerythrocytic growth of Plasmodium falciparum, several parasite proteins are transported from the parasite to the erythrocyte membrane, where they bind to membrane skeletal proteins. Mature-parasite-infected erythrocyte surface antigen (MESA) has previously been shown to associate with host erythrocyte membrane skeletal protein 4.1. Using a spontaneous mutant of P falciparum that has lost the ability to synthesize MESA and 4.1-deficient erythrocytes, we examined growth of MESA(+) and MESA(-) parasites in normal and 4.1-deficient erythrocytes. Viability of MESA(+) parasites was reduc
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46

Roth, E. Jr, V. Joulin, S. Miwa, et al. "The use of enzymopathic human red cells in the study of malarial parasite glucose metabolism." Blood 71, no. 5 (1988): 1408–13. http://dx.doi.org/10.1182/blood.v71.5.1408.1408.

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Abstract The in vitro growth of Plasmodium falciparum malaria parasites was assayed in mutant red cells deficient in either diphosphoglycerate mutase (DPGM) or phosphoglycerate kinase (PGK). In addition, cDNA probes developed for human DNA sequences coding for these enzymes were used to examine the parasite genome by means of restriction endonuclease digestion and Southern blot analysis of parasite DNA. In both types of enzymopathic red cells, parasite growth was normal. In infected DPGM deficient red cells, no DPGM activity could be detected, and in normal red cells, DPGM activity declined sl
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47

Roth, E. Jr, V. Joulin, S. Miwa, et al. "The use of enzymopathic human red cells in the study of malarial parasite glucose metabolism." Blood 71, no. 5 (1988): 1408–13. http://dx.doi.org/10.1182/blood.v71.5.1408.bloodjournal7151408.

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The in vitro growth of Plasmodium falciparum malaria parasites was assayed in mutant red cells deficient in either diphosphoglycerate mutase (DPGM) or phosphoglycerate kinase (PGK). In addition, cDNA probes developed for human DNA sequences coding for these enzymes were used to examine the parasite genome by means of restriction endonuclease digestion and Southern blot analysis of parasite DNA. In both types of enzymopathic red cells, parasite growth was normal. In infected DPGM deficient red cells, no DPGM activity could be detected, and in normal red cells, DPGM activity declined slightly in
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48

Walker, Josephine G., Amy Hurford, Jo Cable, Amy R. Ellison, Stephen J. Price, and Clayton E. Cressler. "Host allometry influences the evolution of parasite host-generalism: theory and meta-analysis." Philosophical Transactions of the Royal Society B: Biological Sciences 372, no. 1719 (2017): 20160089. http://dx.doi.org/10.1098/rstb.2016.0089.

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Parasites vary widely in the diversity of hosts they infect: some parasite species are specialists—infecting just a single host species, while others are generalists, capable of infecting many. Understanding the factors that drive parasite host-generalism is of basic biological interest, but also directly relevant to predicting disease emergence in new host species, identifying parasites that are likely to have unidentified additional hosts, and assessing transmission risk. Here, we use mathematical models to investigate how variation in host body size and environmental temperature affect the
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49

Strauss, Alexander T., Jessica L. Hite, David J. Civitello, Marta S. Shocket, Carla E. Cáceres, and Spencer R. Hall. "Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission." Proceedings of the Royal Society B: Biological Sciences 286, no. 1915 (2019): 20192164. http://dx.doi.org/10.1098/rspb.2019.2164.

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Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. General yet mechanistic models can explain why transmission depends nonlinearly on parasite density and thereby identify potential defensive strategies of hosts. For example, hosts could decrease their exposure rates at higher parasite densities (via behavioural avoidance) or decrease their per-parasite susceptibility when encountering more parasites (e.g. via stronger immune responses). To illustrate, we fitted mechani
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50

Gamboa de Dominguez, ND, and PJ Rosenthal. "Cysteine proteinase inhibitors block early steps in hemoglobin degradation by cultured malaria parasites." Blood 87, no. 10 (1996): 4448–54. http://dx.doi.org/10.1182/blood.v87.10.4448.bloodjournal87104448.

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Erythrocytic malaria parasites degrade hemoglobin as a source of amino acids for parasite protein synthesis. Cysteine proteinase inhibitors have been shown to block the hydrolysis of globin by cultured parasites, indicating that a malarial cysteine proteinase is required for this process. In the present study, we have evaluated the role of parasite proteinases in earlier steps of hemoglobin degradation, namely the disassociation of the hemoglobin tetramer and the separation of heme from globin. Hemoglobin did not spontaneously denature or release heme under the pH and reducing conditions of th
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