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Journal articles on the topic 'Malaria virulence'

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Published: 25 May 2024

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1

Lin, Jing-wen, Adam J. Reid, Deirdre Cunningham, Ulrike Böhme, Irene Tumwine, Sara Keller-Mclaughlin, Mandy Sanders, Matthew Berriman, and Jean Langhorne. "Genomic and transcriptomic comparisons of closely related malaria parasites differing in virulence and sequestration pattern." Wellcome Open Research 3 (November 2, 2018): 142. http://dx.doi.org/10.12688/wellcomeopenres.14797.1.

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Background: Malaria parasite species differ greatly in the harm they do to humans. While P. falciparum kills hundreds of thousands per year, P. vivax kills much less often and P. malariae is relatively benign. Strains of the rodent malaria parasite Plasmodium chabaudi show phenotypic variation in virulence during infections of laboratory mice. This make it an excellent species to study genes which may be responsible for this trait. By understanding the mechanisms which underlie differences in virulence we can learn how parasites adapt to their hosts and how we might prevent disease. Methods: Here we present a complete reference genome sequence for a more virulent P. chabaudi strain, PcCB, and perform a detailed comparison with the genome of the less virulent PcAS strain. Results: We found the greatest variation in the subtelomeric regions, in particular amongst the sequences of the pir gene family, which has been associated with virulence and establishment of chronic infection. However, despite substantial variation at the sequence level, the repertoire of these genes has been largely maintained, highlighting the requirement for functional conservation as well as diversification in host-parasite interactions. However, a subset of pir genes, previously associated with increased virulence, were more highly expressed in PcCB, suggesting a role for this gene family in virulence differences between strains. We found that core genes involved in red blood cell invasion have been under positive selection and that the more virulent strain has a greater preference for reticulocytes, which has elsewhere been associated with increased virulence. Conclusions: These results provide the basis for a mechanistic understanding of the phenotypic differences between Plasmodium chabaudi strains, which might ultimately be translated into a better understanding of malaria parasites affecting humans.
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Lin, Jing-wen, Adam J. Reid, Deirdre Cunningham, Ulrike Böhme, Irene Tumwine, Sara Keller-Mclaughlin, Mandy Sanders, Matthew Berriman, and Jean Langhorne. "Genomic and transcriptomic comparisons of closely related malaria parasites differing in virulence and sequestration pattern." Wellcome Open Research 3 (December 6, 2018): 142. http://dx.doi.org/10.12688/wellcomeopenres.14797.2.

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Background: Malaria parasite species differ greatly in the harm they do to humans. While P. falciparum kills hundreds of thousands per year, P. vivax kills much less often and P. malariae is relatively benign. Strains of the rodent malaria parasite Plasmodium chabaudi show phenotypic variation in virulence during infections of laboratory mice. This make it an excellent species to study genes which may be responsible for this trait. By understanding the mechanisms which underlie differences in virulence we can learn how parasites adapt to their hosts and how we might prevent disease. Methods: Here we present a complete reference genome sequence for a more virulent P. chabaudi strain, PcCB, and perform a detailed comparison with the genome of the less virulent PcAS strain. Results: We found the greatest variation in the subtelomeric regions, in particular amongst the sequences of the pir gene family, which has been associated with virulence and establishment of chronic infection. Despite substantial variation at the sequence level, the repertoire of these genes has been largely maintained, highlighting the requirement for functional conservation as well as diversification in host-parasite interactions. However, a subset of pir genes, previously associated with increased virulence, were more highly expressed in PcCB, suggesting a role for this gene family in virulence differences between strains. We found that core genes involved in red blood cell invasion have been under positive selection and that the more virulent strain has a greater preference for reticulocytes, which has elsewhere been associated with increased virulence. Conclusions: These results provide the basis for a mechanistic understanding of the phenotypic differences between Plasmodium chabaudi strains, which might ultimately be translated into a better understanding of malaria parasites affecting humans.
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3

Deitsch, Kirk W. "Malaria Virulence Genes." Cell 121, no. 1 (April 2005): 1–2. http://dx.doi.org/10.1016/j.cell.2005.03.019.

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4

Schneider, Petra, Andrew S. Bell, Derek G. Sim, Aidan J. O'Donnell, Simon Blanford, Krijn P. Paaijmans, Andrew F. Read, and Sarah E. Reece. "Virulence, drug sensitivity and transmission success in the rodent malaria, Plasmodium chabaudi." Proceedings of the Royal Society B: Biological Sciences 279, no. 1747 (September 26, 2012): 4677–85. http://dx.doi.org/10.1098/rspb.2012.1792.

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Here, we test the hypothesis that virulent malaria parasites are less susceptible to drug treatment than less virulent parasites. If true, drug treatment might promote the evolution of more virulent parasites (defined here as those doing more harm to hosts). Drug-resistance mechanisms that protect parasites through interactions with drug molecules at the sub-cellular level are well known. However, parasite phenotypes associated with virulence might also help parasites survive in the presence of drugs. For example, rapidly replicating parasites might be better able to recover in the host if drug treatment fails to eliminate parasites. We quantified the effects of drug treatment on the in-host survival and between-host transmission of rodent malaria ( Plasmodium chabaudi ) parasites which differed in virulence and had never been previously exposed to drugs. In all our treatment regimens and in single- and mixed-genotype infections, virulent parasites were less sensitive to pyrimethamine and artemisinin, the two antimalarial drugs we tested. Virulent parasites also achieved disproportionately greater transmission when exposed to pyrimethamine. Overall, our data suggest that drug treatment can select for more virulent parasites. Drugs targeting transmission stages (such as artemisinin) may minimize the evolutionary advantage of virulence in drug-treated infections.
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5

Penman, Bridget, and Sunetra Gupta. "Evolution of virulence in malaria." Journal of Biology 7, no. 6 (2008): 22. http://dx.doi.org/10.1186/jbiol83.

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6

Mackinnon, Margaret J., and Andrew F. Read. "Virulence in malaria: an evolutionary viewpoint." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 359, no. 1446 (June 29, 2004): 965–86. http://dx.doi.org/10.1098/rstb.2003.1414.

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Malaria parasites cause much morbidity and mortality to their human hosts. From our evolutionary perspective, this is because virulence is positively associated with parasite transmission rate. Natural selection therefore drives virulence upwards, but only to the point where the cost to transmission caused by host death begins to outweigh the transmission benefits. In this review, we summarize data from the laboratory rodent malaria model, Plasmodium chabaudi , and field data on the human malaria parasite, P. falciparum , in relation to this virulence trade–off hypothesis . The data from both species show strong positive correlations between asexual multiplication, transmission rate, infection length, morbidity and mortality, and therefore support the underlying assumptions of the hypothesis. Moreover, the P. falciparum data show that expected total lifetime transmission of the parasite is maximized in young children in whom the fitness cost of host mortality balances the fitness benefits of higher transmission rates and slower clearance rates, thus exhibiting the hypothesized virulence trade–off. This evolutionary explanation of virulence appears to accord well with the clinical and molecular explanations of pathogenesis that involve cytoadherence, red cell invasion and immune evasion, although direct evidence of the fitness advantages of these mechanisms is scarce. One implication of this evolutionary view of virulence is that parasite populations are expected to evolve new levels of virulence in response to medical interventions such as vaccines and drugs.
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7

Metcalf, C. J. E., G. H. Long, N. Mideo, J. D. Forester, O. N. Bjørnstad, and A. L. Graham. "Revealing mechanisms underlying variation in malaria virulence: effective propagation and host control of uninfected red blood cell supply." Journal of The Royal Society Interface 9, no. 76 (June 20, 2012): 2804–13. http://dx.doi.org/10.1098/rsif.2012.0340.

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Malaria parasite clones with the highest transmission rates to mosquitoes also tend to induce the most severe fitness consequences (or virulence) in mammals. This is in accord with expectations from the virulence–transmission trade-off hypothesis. However, the mechanisms underlying how different clones cause virulence are not well understood. Here, using data from eight murine malaria clones, we apply recently developed statistical methods to infer differences in clone characteristics, including induction of differing host-mediated changes in red blood cell (RBC) supply. Our results indicate that the within-host mechanisms underlying similar levels of virulence are variable and that killing of uninfected RBCs by immune effectors and/or retention of RBCs in the spleen may ultimately reduce virulence. Furthermore, the correlation between clone virulence and the degree of host-induced mortality of uninfected RBCs indicates that hosts increasingly restrict their RBC supply with increasing intrinsic virulence of the clone with which they are infected. Our results demonstrate a role for self-harm in self-defence for hosts and highlight the diversity and modes of virulence of malaria.
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8

Nunes-Alves, Cláudio. "Linking virulence and transmission in malaria." Nature Reviews Microbiology 12, no. 10 (September 8, 2014): 655. http://dx.doi.org/10.1038/nrmicro3354.

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9

Mancio-Silva, Liliana, Ksenija Slavic, Margarida T. Grilo Ruivo, Ana Rita Grosso, Katarzyna K. Modrzynska, Iset Medina Vera, Joana Sales-Dias, et al. "Nutrient sensing modulates malaria parasite virulence." Nature 547, no. 7662 (July 2017): 213–16. http://dx.doi.org/10.1038/nature23009.

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10

Chookajorn, Thanat, Ron Dzikowski, Matthias Frank, Felomena Li, Alisha Z. Jiwani, Daniel L. Hartl, and Kirk W. Deitsch. "Epigenetic memory at malaria virulence genes." Proceedings of the National Academy of Sciences 104, no. 3 (January 5, 2007): 899–902. http://dx.doi.org/10.1073/pnas.0609084103.

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11

Otsuki, Hitoshi, Osamu Kaneko, Amporn Thongkukiatkul, Mayumi Tachibana, Hideyuki Iriko, Satoru Takeo, Takafumi Tsuboi, and Motomi Torii. "Single amino acid substitution inPlasmodium yoeliierythrocyte ligand determines its localization and controls parasite virulence." Proceedings of the National Academy of Sciences 106, no. 17 (April 3, 2009): 7167–72. http://dx.doi.org/10.1073/pnas.0811313106.

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The major virulence determinant of the rodent malaria parasite,Plasmodium yoelii, has remained unresolved since the discovery of the lethal line in the 1970s. Because virulence in this parasite correlates with the ability to invade different types of erythrocytes, we evaluated the potential role of the parasite erythrocyte binding ligand,PyEBL. We found 1 amino acid substitution in a domain responsible for intracellular trafficking between the lethal and nonlethal parasite lines and, furthermore, that the intracellular localization ofPyEBL was distinct between these lines. Genetic modification showed that this substitution was responsible not only forPyEBL localization but also the erythrocyte-type invasion preference of the parasite and subsequently its virulence in mice. This previously unrecognized mechanism for altering an invasion phenotype indicates that subtle alterations of a malaria parasite ligand can dramatically affect host–pathogen interactions and malaria virulence.
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12

Uskov, A. N., A. I. Soloviev, V. Yu Kravtsov, R. V. Gudkov, E. V. Kolomoets, and A. E. Levkovskiy. "MOLECULAR-GENETIC MECHANISMS OF PLASMODIUM FALCIPARUM VIRULENCE AND TROPICAL MALARIA PATHOGENESIS." Journal Infectology 10, no. 3 (October 7, 2018): 23–29. http://dx.doi.org/10.22625/2072-6732-2018-10-3-23-29.

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There is introduced the analysis of molecular-genetic mechanisms of tropical malaria pathogenesis and P. falciparum virulence. It is shown, that pathogenesis of tropical malaria is associated with the properties of red blood cells membrane surface (RBCs or erythrocytes) that are infected by P. falciparum. There are «knobs structures» on membrane surface infected RBCs. Knobs structures contains a complex of P. falciparum proteins – PfEMP1 (Plasmodium falciparum erythrocyte membrane protein 1). PfEMP1 is associated with virulence of P. falciparum. Complex PfEMP1 has difficult polymorphous structure. Domains of PfEMP1 are able to associate with different cell receptors. Virulence`s individual components of the main factor are selectively sensitive to different tissues and organs. The severity of the clinical malaria infection course depends on the complex structure PfEMP1 of malaria parasites. Composition of polypeptide PfEMP1 is determined by var-complex. Nowadays there are 60 variants of var-complex. Regulation of gene expression, forming part of the var-complex, is carried out on a molecular-genetic level, cellular level, tissue level. Modern research in this area are aimed to explore genes polymorphism of the virulence`s main factor, to identify mechanism of its differential expression. Search of molecular – genetic markers is relevant to develop methods of gene diagnostic and malaria vaccine.
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13

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 (July 6, 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 measures) and how this may impact the virulence of the circulating parasites. To this end, we have built an individual-based model that captures the main selective forces on malaria parasites, namely parasite competition, host immunity, host death and mosquito abundance at both the within- and between-host levels. VSAs are defined by the net growth rates they infer to the parasites and the model keeps track of the expression of, and antibody build-up against, each VSA in all hosts. Our results show an ordered acquisition of VSA-specific antibodies with host age, which causes a dichotomy between the more virulent VSAs that reach high parasitaemias but are restricted to young relatively non-immune hosts, and less virulent VSAs that do not reach such high parasitaemias but can infect a wider range of hosts. The outcome of a change in the parasite's environment in terms of parasite virulence depends on the exact balance between the selection forces, which sets the limiting factor for parasite survival. Parasites will evolve towards expressing more virulent VSAs when the limiting factor for parasite survival is the within-host parasite growth and the parasites are able to minimize this limitation by expressing more virulent VSAs.
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14

Targett, G. A. T. "Virulence and the immune response in malaria." Memórias do Instituto Oswaldo Cruz 87, suppl 5 (1992): 137–44. http://dx.doi.org/10.1590/s0074-02761992000900022.

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15

Stein, Wilfred D., Cecilia P. Sanchez, and Michael Lanzer. "Virulence and drug resistance in malaria parasites." Trends in Parasitology 25, no. 10 (October 2009): 441–43. http://dx.doi.org/10.1016/j.pt.2009.07.003.

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16

Nauriyal, Deepty, and Deepak Kumar. "Study of Severe Malaria Caused by Plasmodium Vivax in Comparison to Plasmodium Falciparum and Mixed Malarial Infections in Children." Biomedical and Pharmacology Journal 15, no. 3 (September 29, 2022): 1597–604. http://dx.doi.org/10.13005/bpj/2498.

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Background: Malaria alone is responsible for major proportion of morbidity and mortality in children. Most cases of malaria are due to P.vivax. P.vivax has always been considered benign but recent studies and molecular studies are giving evidences towards increasing virulence and severity of P.vivax Aims and objective: Aim of this study was to observe severe malaria caused by P.vivax in comparison to Falciparum and mixed malarial infections. Other added aim was to observe for concomitant bacterial infections, how it affects clinical outcome and role of antibiotics in such cases of severe malaria. Materials and methods: This was a hospital based study conducted in a tertiary care center in Uttar Pradesh. Patients were tested for malaria using Peripheral blood smear and Rapid malaria antigen test. Total of 200 cases of severe malaria were enrolled in study. Patients were categorized as severe malaria on basis of WHO guidelines. Results: Of 200 cases of severe malaria, 130 (65%) had P.vivax infection, 31 (15.5%) had falciparum infection and 39 (19.5%) had mixed infection with both the species. Noteworthy results observed in cases of severe malaria with P.vivax infections were cerebral malaria (29.2%), severe anemia (26.9 %), severe thrombocytopenia (7.6%) and mortality (13%). Almost 15 % of total patients had concomitant bacterial infections that contributed significantly towards morbidity and prolonged hospitalization. Conclusion: From our study we observed that P.vivax cannot more be considered benign and needs quick diagnosis, prompt treatment and should be observed for complications. Antibiotics use should be considered in severe malaria.
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Ch’ng, Jun-Hong, Kirsten Moll, Katja Wyss, Ulf Hammar, Mikael Rydén, Olle Kämpe, Anna Färnert, and Mats Wahlgren. "Enhanced virulence of Plasmodium falciparum in blood of diabetic patients." PLOS ONE 16, no. 6 (June 17, 2021): e0249666. http://dx.doi.org/10.1371/journal.pone.0249666.

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Rising prevalence of diabetes in sub-Saharan Africa, coupled with continued malaria transmission, has resulted more patients dealing with both communicable and non-communicable diseases. We previously reported that travelers with type 2 diabetes mellitus (T2DM) infected with Plasmodium falciparum were three times more likely to develop severe malaria than non-diabetics. Here we explore the biological basis for this by testing blood from uninfected subjects with type 1 and type 2 diabetes, ex vivo, for their effects on parasite growth and rosetting (binding of infected erythrocytes to uninfected erythrocytes). Rosetting was associated with type 2 diabetes, blood glucose and erythrocyte sedimentation rate (ESR), while parasite growth was positively associated with blood glucose, glycated hemoglobin (HbA1c), body mass index (BMI), fibrinogen and triglycerides. This study establishes a link between diabetes and malaria virulence assays, potentially explaining the protective effect of good glycemic control against severe malaria in subjects with diabetes.
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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 (March 27, 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 tissue vasculature is dependent on the PTEX components thioredoxin 2 (TRX2) and PTEX88. While TRX2 -deficient parasites remain virulent, PTEX88 -deficient parasites no longer sequester in the brain, correlating with abolishment of cerebral complications in infected mice. However, an apparent trade-off for virulence attenuation was spleen enlargement, which correlates with a strongly reduced schizont-to-ring-stage transition. Strikingly, general protein export is unaffected in PTEX88 -deficient mutants that mature normally in vitro . Thus, PTEX88 is pivotal for tissue sequestration in vivo , parasite virulence, and preventing exacerbation of spleen pathology, but these functions do not correlate with general protein export to the host erythrocyte. The presented data suggest that the protein export machinery of Plasmodium parasites and their underlying mechanistic features are considerably more complex than previously anticipated and indicate challenges for targeted intervention strategies.
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PRAJAPATI, SURENDRA KUMAR, and OM PRAKASH SINGH. "Identification of avir-orthologous immune evasion gene family from primate malaria parasites." Parasitology 141, no. 5 (January 27, 2014): 641–45. http://dx.doi.org/10.1017/s003118201300214x.

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SUMMARYThe immune evasion gene family of malaria parasites encodes variant surface proteins that are expressed at the surface of infected erythrocytes and help the parasite in evading the host immune response by means of antigenic variation. The identification ofPlasmodium vivax virorthologous immune evasion gene family from primate malaria parasites would provide new insight into the evolution of virulence and pathogenesis. Threevirsubfamilies viz.vir-B, vir-Dandvir-Gwere successfully PCR amplified from primate malaria parasites, cloned and sequenced. DNA sequence analysis confirmed orthologues ofvir-Dsubfamily inPlasmodium cynomolgi, Plasmodium simium, Plasmodium simiovaleandPlasmodium fieldi. The identifiedvir-Dorthologues are 1–9 distinct members of the immune evasion gene family which have 68–83% sequence identity withvir-Dand 71·2–98·5% sequence identity within the members identified from primate malaria parasites. The absence of othervirsubfamilies among primate malaria parasites reflects the limitations in the experimental approach. This study clearly identified the presence ofvir-Dlike sequences in four species ofPlasmodiuminfecting primates that would be useful in understanding the evolution of virulence in malaria parasites.
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20

Marti, Matthias, Jake Baum, Melanie Rug, Leann Tilley, and Alan F. Cowman. "Signal-mediated export of proteins from the malaria parasite to the host erythrocyte." Journal of Cell Biology 171, no. 4 (November 21, 2005): 587–92. http://dx.doi.org/10.1083/jcb.200508051.

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Intracellular parasites from the genus Plasmodium reside and multiply in a variety of cells during their development. After invasion of human erythrocytes, asexual stages from the most virulent malaria parasite, P. falciparum, drastically change their host cell and export remodelling and virulence proteins. Recent data demonstrate that a specific NH2-terminal signal conserved across the genus Plasmodium plays a central role in this export process.
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21

Ferguson, H. M., M. J. Mackinnon, B. H. Chan, and A. F. Read. "MOSQUITO MORTALITY AND THE EVOLUTION OF MALARIA VIRULENCE." Evolution 57, no. 12 (2003): 2792. http://dx.doi.org/10.1554/03-211.

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Mackinnon, Margaret J., and Andrew F. Read. "Immunity Promotes Virulence Evolution in a Malaria Model." PLoS Biology 2, no. 9 (June 22, 2004): e230. http://dx.doi.org/10.1371/journal.pbio.0020230.

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Ferguson, H. M., M. J. Mackinnon, B. H. Chan, and A. F. Read. "MOSQUITO MORTALITY AND THE EVOLUTION OF MALARIA VIRULENCE." Evolution 57, no. 12 (December 2003): 2792–804. http://dx.doi.org/10.1111/j.0014-3820.2003.tb01521.x.

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24

Flueck, Christian, and David A. Baker. "Malaria Parasite Epigenetics: When Virulence and Romance Collide." Cell Host & Microbe 16, no. 2 (August 2014): 148–50. http://dx.doi.org/10.1016/j.chom.2014.07.012.

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25

Bernabeu, Maria, Samuel A. Danziger, Marion Avril, Marina Vaz, Prasad H. Babar, Andrew J. Brazier, Thurston Herricks, et al. "Severe adult malaria is associated with specific PfEMP1 adhesion types and high parasite biomass." Proceedings of the National Academy of Sciences 113, no. 23 (May 16, 2016): E3270—E3279. http://dx.doi.org/10.1073/pnas.1524294113.

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The interplay between cellular and molecular determinants that lead to severe malaria in adults is unexplored. Here, we analyzed parasite virulence factors in an infected adult population in India and investigated whether severe malaria isolates impair endothelial protein C receptor (EPCR), a protein involved in coagulation and endothelial barrier permeability. Severe malaria isolates overexpressed specific members of the Plasmodium falciparum var gene/PfEMP1 (P. falciparum erythrocyte membrane protein 1) family that bind EPCR, including DC8 var genes that have previously been linked to severe pediatric malaria. Machine learning analysis revealed that DC6- and DC8-encoding var transcripts in combination with high parasite biomass were the strongest indicators of patient hospitalization and disease severity. We found that DC8 CIDRα1 domains from severe malaria isolates had substantial differences in EPCR binding affinity and blockade activity for its ligand activated protein C. Additionally, even a low level of inhibition exhibited by domains from two cerebral malaria isolates was sufficient to interfere with activated protein C-barrier protective activities in human brain endothelial cells. Our findings demonstrate an interplay between parasite biomass and specific PfEMP1 adhesion types in the development of adult severe malaria, and indicate that low impairment of EPCR function may contribute to parasite virulence.
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Schall, J. J. "Virulence of lizard malaria: the evolutionary ecology of an ancient parasite—host association." Parasitology 100, S1 (June 1990): S35—S52. http://dx.doi.org/10.1017/s0031182000073005.

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SummaryThe negative consequences of parasitic infection (virulence) were examined for two lizard malaria parasite—host associa tions: Plasmodium agamae and P. giganteum, parasites of the rainbow lizard, Agama agania, in Sierra Leone, West Africa; and P. mexicanum in the western fence lizard, Sceloporus occidentalis, in northern California. These malaria species vary greatly in their reproductive characteristics: P. agamae produces only 8 merozoites per schizont, P. giganteum yields over 100, and P. mexicanum an intermediate number. All three parasites appear to have had an ancient association with their host. In fence lizards, infection with malaria is associated with increased numbers of immature erythrocytes, decreased haemoglobin levels, decreased maximal oxygen consumption, and decreased running stamina. Not affected were numbers of erythrocytes, resting metabolic rate, and sprint running speed which is supported by anaerobic means in lizards. Infected male fence lizards had smaller testes, stored less fat in preparation for winter dormancy, were more often socially submissive and, unexpectedly, were more extravagantly coloured on the ventral surface (a sexually dimorphic trait) than non-infected males. Females also stored less fat and produced smaller clutches of eggs, a directly observed reduction in fitness. Infected fence lizards do not develop behavioural fevers. P. mexicanum appears to have broad thermal buffering abilities and thermal tolerance; the parasite's population growth was unaffected by experimental alterations in the lizard's body temperature. The data are less complete for A. agama, but infected lizards suffered similar haematological and physiological effects. Infected animals may be socially submissive because they appear to gather less insect prey, possibly a result of being forced into inferior territories. Infection does not reduce clutch size in rainbow lizards, but may lengthen the time between clutches. These results are compared with predictions emerging from several models of the evolution of parasite virulence. The lack of behavioural fevers in fence lizards may represent a physiological constraint by the lizards in evolving a thermal tolerance large enough to allow elimination of the parasite via fever. Such constraints may be important in determining the outcome of parasite—host coevolution. Some theory predicts low virulence in old parasite—host systems and higher virulence in parasites with greater reproductive output. However, in conflict with this argument, all three malarial species exhibited similar high costs to their hosts.
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Butcher, G. A., and I. A. Clark. "The inhibition ofPlasmodium falciparumgrowthin vitroby sera from mice infected with malaria or treated with TNF." Parasitology 101, no. 3 (December 1990): 321–26. http://dx.doi.org/10.1017/s0031182000060509.

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SUMMARYDespite some years of enquiry, the mechanism that leads to intra-erythrocytic death of malarial parasites during the host's response to infection has not been elucidated. We report here that serum from mice undergoing a successful immune response toPlasmodium chabaudidoes not inhibitPlasmodium falciparumunless thePl. chabaudiis virulent enough to rise to at least 50% parasitaemia and to cause illness. This appears to be true of the 556 KA and DS strains ofPl chabaudi, and also other murine malaria parasites. In mice infected withPl. chabaudi556 KA inhibitory activity coincided with the presence of TNF in their serum. Exogenous TNF generated inhibitory activity in the serum of mice only if the animals were pretreated withProprionobacterium acnes, implying a role for activated macrophages downstream from TNF in this process. The difference in inhibitory activity againstPl. falciparumin serum from mice infected withPl. chabaudiof more or less virulence may be one of degree. Alternatively two distinct mechanisms may operate, the second coming into operation only in ill mice, with higher parasite burdens.
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28

Gonçalves, Raquel Müller, Nathália Ferreira Lima, and Marcelo Urbano Ferreira. "Parasite virulence, co-infections and cytokine balance in malaria." Pathogens and Global Health 108, no. 4 (May 23, 2014): 173–78. http://dx.doi.org/10.1179/2047773214y.0000000139.

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29

Gupta, S., A. V. Hill, D. Kwiatkowski, A. M. Greenwood, B. M. Greenwood, and K. P. Day. "Parasite virulence and disease patterns in Plasmodium falciparum malaria." Proceedings of the National Academy of Sciences 91, no. 9 (April 26, 1994): 3715–19. http://dx.doi.org/10.1073/pnas.91.9.3715.

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30

Fatih, Farrah A., Angela Siner, Atique Ahmed, Lu Woon, Alister G. Craig, Balbir Singh, Sanjeev Krishna, and Janet Cox-Singh. "Cytoadherence and virulence - the case of Plasmodium knowlesi malaria." Malaria Journal 11, no. 1 (2012): 33. http://dx.doi.org/10.1186/1475-2875-11-33.

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31

de Roode, J. C., R. Pansini, S. J. Cheesman, M. E. H. Helinski, S. Huijben, A. R. Wargo, A. S. Bell, B. H. K. Chan, D. Walliker, and A. F. Read. "Virulence and competitive ability in genetically diverse malaria infections." Proceedings of the National Academy of Sciences 102, no. 21 (May 13, 2005): 7624–28. http://dx.doi.org/10.1073/pnas.0500078102.

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32

Larcombe, Stephen D., Stéphanie Bedhomme, Stéphane Garnier, Elise Cellier-Holzem, Bruno Faivre, and Gabriele Sorci. "Social interactions modulate the virulence of avian malaria infection." International Journal for Parasitology 43, no. 10 (September 2013): 861–67. http://dx.doi.org/10.1016/j.ijpara.2013.05.008.

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33

MACKINNON, M. J., and A. F. READ. "The effects of host immunity on virulence–transmissibility relationships in the rodent malaria parasite Plasmodium chabaudi." Parasitology 126, no. 2 (February 2003): 103–12. http://dx.doi.org/10.1017/s003118200200272x.

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Here we examined the impact of host immunity on relationships between parasite virulence, transmission rate, intrinsic growth rate and host recovery rate in the rodent malaria parasite, Plasmodium chabaudi. Groups of naïve and immunized mice were infected with 1 of 10 cloned lines of parasites and their infection dynamics were monitored for 19 days. We found that (1) host immunity reduced the growth rate, virulence, transmission rate and infection length, with a consequent 3-fold reduction in life-time transmission potential, (2) clone means for these traits ranked similarly across naïve and immunized mice, (3) regression slopes of transmission potential on growth rate, virulence and infection length were similar in naïve and immunized mice, (4) virulence and infection length were positively correlated in immunized but not naïve mice, and (5) for a similar level of parasite growth rate and virulence, transmission potential and infection length were lower in immunized than naïve mice. Thus host immunity reduced all these fitness traits in a manner consistent with direct parasite-driven biological links among them. These results support the basic assumption underlying our theory that predicts that anti-disease vaccines will select for higher virulence in those microparasites for which virulence is integrally linked to transmission.
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34

Baruch, Dror I., Xin C. Ma, Hardeep B. Singh, Xiahui Bi, Brittan L. Pasloske, and Russell J. Howard. "Identification of a Region of PfEMP1 That Mediates Adherence of Plasmodium falciparum Infected Erythrocytes to CD36: Conserved Function With Variant Sequence." Blood 90, no. 9 (November 1, 1997): 3766–75. http://dx.doi.org/10.1182/blood.v90.9.3766.

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Abstract Adherence of mature parasitized erythrocytes (PE) of Plasmodium falciparum to microvascular endothelial cells contributes directly to the virulence and pathology of this human malaria. The malarial variant antigen, P falciparum erythrocyte membrane protein 1 (PfEMP1), has been implicated as the PE receptor for CD36 on endothelial cells. We identified the region of PfEMP1 that mediates adherence of PE to CD36 and showed that a recombinant protein fragment from this region blocked and reversed adherence of antigenically different parasites. Sequence variation was evident in the CD36 binding domain of different PfEMP1 genes, yet many highly conserved residues, particularly cysteine residues, are evident. This suggests a highly conserved shape that mediates adherence to CD36. Immunization with the CD36-binding domain elicited sera that are cross-reactive with the different recombinant proteins but are strain-specific for the PE surface. Novel anti-adherence therapeutics and a malaria vaccine may derived from exploitation of the structure of the CD36 binding domain of PfEMP1.
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35

Bunnik, Evelien M., Aarthi Venkat, Jianlin Shao, Kathryn E. McGovern, Gayani Batugedara, Danielle Worth, Jacques Prudhomme, et al. "Comparative 3D genome organization in apicomplexan parasites." Proceedings of the National Academy of Sciences 116, no. 8 (February 5, 2019): 3183–92. http://dx.doi.org/10.1073/pnas.1810815116.

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The positioning of chromosomes in the nucleus of a eukaryotic cell is highly organized and has a complex and dynamic relationship with gene expression. In the human malaria parasite Plasmodium falciparum, the clustering of a family of virulence genes correlates with their coordinated silencing and has a strong influence on the overall organization of the genome. To identify conserved and species-specific principles of genome organization, we performed Hi-C experiments and generated 3D genome models for five Plasmodium species and two related apicomplexan parasites. Plasmodium species mainly showed clustering of centromeres, telomeres, and virulence genes. In P. falciparum, the heterochromatic virulence gene cluster had a strong repressive effect on the surrounding nuclear space, while this was less pronounced in Plasmodium vivax and Plasmodium berghei, and absent in Plasmodium yoelii. In Plasmodium knowlesi, telomeres and virulence genes were more dispersed throughout the nucleus, but its 3D genome showed a strong correlation with gene expression. The Babesia microti genome showed a classical Rabl organization with colocalization of subtelomeric virulence genes, while the Toxoplasma gondii genome was dominated by clustering of the centromeres and lacked virulence gene clustering. Collectively, our results demonstrate that spatial genome organization in most Plasmodium species is constrained by the colocalization of virulence genes. P. falciparum and P. knowlesi, the only two Plasmodium species with gene families involved in antigenic variation, are unique in the effect of these genes on chromosome folding, indicating a potential link between genome organization and gene expression in more virulent pathogens.
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TIMMS, R., N. COLEGRAVE, B. H. K. CHAN, and A. F. READ. "The effect of parasite dose on disease severity in the rodent malaria Plasmodium chabaudi." Parasitology 123, no. 1 (July 2001): 1–11. http://dx.doi.org/10.1017/s0031182001008083.

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Experiments were designed to look at the relationship between infective dose and disease severity using 2 clones of Plasmodium chabaudi that differ in virulence. We asked whether there were dose–severity relationships, whether clone differences in virulence were maintained over a range of doses, and whether disease severity could be accounted for by parasite dynamics. Groups of mice were infected with parasite doses differing by an order of magnitude, ranging from 100 to 1×108 parasites. Infective dose affected the probability of death, but only with the more virulent clone. Dose also affected morbidity. For both clones, higher doses induced greater anaemia. Larger doses caused greater weight loss, but only for infections with the more virulent clone. Here, for a given dose, mice lost a fixed amount of weight, irrespective of their initial weight. Larger doses induced earlier mortality and morbidity than did lower dose treatments. Finally, dose affected parasite dynamics, with earlier and higher peak parasite densities in larger dose infections. All these effects were small relative to clone differences in disease severity, which were apparent across the range of doses. Dose effects were manifested through the timing and/or magnitude of peak parasite densities, broadly supporting the idea that dose affects disease severity by altering the time the host has to control parasite densities and ameliorate the effects of parasites. We discuss the possible efficacy of intervention strategies aimed at reducing human disease severity by reducing infective parasite dose.
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Clarebout, G., B. Gamain, C. Slomianny, D. Camus, and D. Dive. "The course ofPlasmodium berghei, P. chabaudiandP. yoeliiinfections in β-thalassaemic mice." Parasitology 112, no. 3 (March 1996): 269–76. http://dx.doi.org/10.1017/s0031182000065781.

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SUMMARYIn order to study the effects of acclimatization ofPlasmodiumin β-thalassaemic mice, we used a mouse model of β-thalassaemia (DBA/2J/β-thal/β-thal), similar to that observed in humans. We acclimatized 3 rodent malarias (P. berghei, P. chabaudiandP. yoelii) in DBA/2J and DBA/2J/β-thal/β-thal mice lines, by 4 intraperitoneal serial transfers. All 3 rodent malarias developed in red blood cells of β-thalassaemic mice without losing their virulence. There was no delay in infection and peaks of parasitaemia were similar in β-thalassaemic and normal mice. The mortality occurred earlier in β-thalassaemic mice than in control mice forP. bergheiandP. chabaudi. This difference was more pronounced forP. yoeliiNS where normal mice did not die. These results could be explained by a failure of erythropoiesis in β-thalassaemic mice, which are unable to compensate for the destruction of red blood cells by the parasites, and the mice died of anaemia. Ultrastructural examination of the rodent malaria parasites in β-thalassaemic RBC showed a normal development even in the presence of Heinz bodies. In conclusion, no effective protection against malaria was provided by the β-thalassaemia in this mouse model.
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Nguetse, Christian N., Natasha Purington, Emily R. Ebel, Bikash Shakya, Marilou Tetard, Peter G. Kremsner, Thirumalaisamy P. Velavan, and Elizabeth S. Egan. "A common polymorphism in the mechanosensitive ion channel PIEZO1 is associated with protection from severe malaria in humans." Proceedings of the National Academy of Sciences 117, no. 16 (April 7, 2020): 9074–81. http://dx.doi.org/10.1073/pnas.1919843117.

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Malaria caused by the apicomplexan parasite Plasmodium falciparum has served as a strong evolutionary force throughout human history, selecting for red blood cell polymorphisms that confer innate protection against severe disease. Recently, gain-of-function mutations in the mechanosensitive ion channel PIEZO1 were shown to ameliorate Plasmodium parasite growth, blood–brain barrier dysfunction, and mortality in a mouse model of malaria. In humans, the gain-of-function allele PIEZO1 E756del is highly prevalent and enriched in Africans, raising the possibility that it is under positive selection due to malaria. Here we used a case-control study design to test for an association between PIEZO1 E756del and malaria severity among children in Gabon. We found that the E756del variant is strongly associated with protection against severe malaria in heterozygotes. In subjects with sickle cell trait, heterozygosity for PIEZO1 E756del did not confer additive protection and homozygosity was associated with an elevated risk of severe disease, suggesting an epistatic relationship between hemoglobin S and PIEZO1 E756del. Using donor blood samples, we show that red cells heterozygous for PIEZO1 E756del are not dehydrated and can support the intracellular growth of P. falciparum similar to wild-type cells. However, surface expression of the P. falciparum virulence protein PfEMP-1 was significantly reduced in infected cells heterozygous for PIEZO1 756del, a phenomenon that has been observed with other protective polymorphisms, such as hemoglobin C. Our findings demonstrate that PIEZO1 is an important innate determinant of malaria susceptibility in humans and suggest that the mechanism of protection may be related to impaired export of P. falciparum virulence proteins.
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39

Riley, E. M. "The role of MHC- and non-MHC-associated genes in determining the human immune response to malaria antigens." Parasitology 112, S1 (March 1996): S39—S51. http://dx.doi.org/10.1017/s0031182000076654.

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SUMMARYIndividual susceptibility to malaria infection, disease and death is influenced by host genotype, parasite virulence and a number of environmental factors including malaria-specific immunity. Immune responses are themselves determined by a combination of host genes and environmental effects. The extent to which host genotype limits the spectrum of possible immune responses may influence the outcome of infection and has consequences for vaccine design. Associations have been observed between human major histocompatibility complex (MHC) genotype and susceptibility to severe malaria, but no similar associations have been observed for mild malarial disease or for specific antibody responses to defined malaria antigens. Epidemiological studies have shown that, in practice, neither T helper cell nor antibody responses to malaria parasites are limited by host MHC genotype, but have revealed that genes lying outside the MHC may influence T cell proliferative responses. These genes have yet to be identified, but possible candidates include T cell receptor (TcR) genes, and genes involved in TcR gene rearrangements. More importantly, perhaps, longitudinal epidemiological studies have shown that the anti-malarial antibody repertoire is selective and becomes fixed in malaria-immune individuals, but is independent of host genotype. These findings suggest that the antibody repertoire may be determined, at least in part, by stochastic events. The first of these is the generation of the T and B cell repertoire, which results from random gene recombinations and somatic mutation and is thus partially independent of germline genes. Secondly, of the profusion of immunogenic peptides which are processed and presented by antigen presenting cells, a few will, by chance, interact with T and B cell surface antigen receptors of particularly high affinity. These T and B cell clones will be selected, will expand and may come to dominate the immune response, preventing the recognition of variant epitopes presented by subsequent infections - a process known as original antigenic sin or clonal imprinting. The immune response of an individual thus reflects the balance between genetic and stochastic effects. This may have important consequences for subunit vaccine development.
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40

Lenz, Todd, and Karine G. Le Roch. "Three-Dimensional Genome Organization and Virulence in Apicomplexan Parasites." Epigenetics Insights 12 (January 2019): 251686571987943. http://dx.doi.org/10.1177/2516865719879436.

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Mounting evidence supports the idea that epigenetic, and the overall 3-dimensional (3D) architecture of the genome, plays an important role in gene expression for eukaryotic organisms. We recently used Hi-C methodologies to generate and compare the 3D genome of 7 different apicomplexan parasites, including several pathogenic and less pathogenic malaria parasites as well as related human parasites Babesia microti and Toxoplasma gondii. Our goal was to understand the possible relationship between genome organization, gene expression, and pathogenicity of these infectious agents. Collectively, our results demonstrate that spatial genome organization in most Plasmodium species is constrained by the colocalization of virulence genes that are unique in their effect on chromosome folding, indicating a link between genome organization and gene expression in more virulent pathogens.
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41

Mackinnon, M. J., and A. Read. "Selection for high and low virulence in the malaria parasite." Proceedings of the Royal Society of London. Series B: Biological Sciences 266, no. 1420 (April 7, 1999): 741–48. http://dx.doi.org/10.1098/rspb.1999.0699.

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42

Ferguson, H. M., and A. F. Read. "Genetic and environmental determinants of malaria parasite virulence in mosquitoes." Proceedings of the Royal Society of London. Series B: Biological Sciences 269, no. 1497 (June 22, 2002): 1217–24. http://dx.doi.org/10.1098/rspb.2002.2023.

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43

Marti, M. "Targeting Malaria Virulence and Remodeling Proteins to the Host Erythrocyte." Science 306, no. 5703 (December 10, 2004): 1930–33. http://dx.doi.org/10.1126/science.1102452.

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44

Mackinnon, M. J., D. J. Gaffney, and A. F. Read. "Virulence in rodent malaria: host genotype by parasite genotype interactions." Infection, Genetics and Evolution 1, no. 4 (July 2002): 287–96. http://dx.doi.org/10.1016/s1567-1348(02)00039-4.

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45

Deitsch, Kirk W., and Lars Hviid. "Variant surface antigens, virulence genes and the pathogenesis of malaria." Trends in Parasitology 20, no. 12 (December 2004): 562–66. http://dx.doi.org/10.1016/j.pt.2004.09.002.

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46

Mackinnon, M. J., S. Gandon, and A. F. Read. "Virulence evolution in response to vaccination: The case of malaria." Vaccine 26 (July 2008): C42—C52. http://dx.doi.org/10.1016/j.vaccine.2008.04.012.

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47

Holding, Thomas, and Mario Recker. "Maintenance of phenotypic diversity within a set of virulence encoding genes of the malaria parasite Plasmodium falciparum." Journal of The Royal Society Interface 12, no. 113 (December 2015): 20150848. http://dx.doi.org/10.1098/rsif.2015.0848.

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Infection by the human malaria parasite Plasmodium falciparum results in a broad spectrum of clinical outcomes, ranging from severe and potentially life-threatening malaria to asymptomatic carriage. In a process of naturally acquired immunity, individuals living in malaria-endemic regions build up a level of clinical protection, which attenuates infection severity in an exposure-dependent manner. Underlying this shift in the immunoepidemiology as well as the observed range in malaria pathogenesis is the var multigene family and the phenotypic diversity embedded within. The var gene-encoded surface proteins Plasmodium falciparum erythrocyte membrane protein 1 mediate variant-specific binding of infected red blood cells to a diverse set of host receptors that has been linked to specific disease manifestations, including cerebral and pregnancy-associated malaria. Here, we show that cross-reactive immune responses, which minimize the within-host benefit of each additionally expressed gene during infection, can cause selection for maximum phenotypic diversity at the genome level. We further show that differential functional constraints on protein diversification stably maintain uneven ratios between phenotypic groups, in line with empirical observation. Our results thus suggest that the maintenance of phenotypic diversity within P. falciparum is driven by an evolutionary trade-off that optimizes between within-host parasite fitness and between-host selection pressure.
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48

Belachew, Esmael Besufikad. "Immune Response and Evasion Mechanisms of Plasmodium falciparum Parasites." Journal of Immunology Research 2018 (2018): 1–6. http://dx.doi.org/10.1155/2018/6529681.

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Malaria causes approximately 212 million cases and 429 thousand deaths annually. Plasmodium falciparum is responsible for the vast majority of deaths (99%) than others. The virulence of P. falciparum is mostly associated with immune response-evading ability. It has different mechanisms to evade both Anopheles mosquito and human host immune responses. Immune-evading mechanisms in mosquito depend mainly on the Pfs47 gene that inhibits Janus kinase-mediated activation. Host complement factor also protects human complement immune attack of extracellular gametes in Anopheles mosquito midgut. In the human host, evasion largely results from antigenic variation, polymorphism, and sequestration. They also induce Kupffer cell apoptosis at the preerythrocytic stage and interfere with phagocytic functions of macrophage by hemozoin in the erythrocytic stage. Lack of major histocompatibility complex-I molecule expression on the surface red blood cells also avoids recognition by CD8+ T cells. Complement proteins could allow for the entry of parasite into the red blood cell. Intracellular survival also assists the escape of malarial parasite. Invading, evading, and immune response mechanisms both in malaria vector and human host are critical to design appropriate vaccine. As a result, the receptors and ligands involved in different stages of malaria parasites should be elucidated.
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van der Heyde, H. C., D. D. Manning, D. C. Roopenian, and W. P. Weidanz. "Resolution of blood-stage malarial infections in CD8+ cell-deficient beta 2-m0/0 mice." Journal of Immunology 151, no. 6 (September 15, 1993): 3187–91. http://dx.doi.org/10.4049/jimmunol.151.6.3187.

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Abstract We utilized a definitive model of CD8+ T cell deficiency, the beta 2-microglobulin-deficient (beta 2-m0/0) mouse, to determine whether CD8+ T cells are required in the resolution of blood-stage malaria. In a parallel experiment, C57Bl/6 mice treated with anti-CD8 mAb showed significantly higher levels of parasitemia than untreated C57Bl/6 control mice at several points during the infection. This finding suggests some role for CD8+ cells in containing malaria. However, the beta 2-m0/0 mice, which are genetically blocked from expressing MHC class I or class Ib glycoproteins and therefore have < 2.5% of the normal number of CD8+ T cells, nevertheless resolved infections with three virulence variants of murine Plasmodium. The resolution of Plasmodium chabaudi adami, Plasmodium yoelii yoelii 17X, and Plasmodium chabaudi chabaudi AS infections by beta 2-m0/0 mice in the virtual absence of CD8+ cells demonstrates that these cells are not required to suppress murine malaria and that the suppression mechanism is not MHC class I restricted. The similarity of the time-course for resolution of infection in beta 2-m0/0 and intact control mice with all three subspecies of Plasmodium further supports the lack of a requirement for CD8+ T cells in the suppression of malarial parasitemia.
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50

Wargo, Andrew R., Jacobus C. de Roode, Silvie Huijben, Damien R. Drew, and Andrew F. Read. "Transmission stage investment of malaria parasites in response to in-host competition." Proceedings of the Royal Society B: Biological Sciences 274, no. 1625 (August 21, 2007): 2629–38. http://dx.doi.org/10.1098/rspb.2007.0873.

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Conspecific competition occurs in a multitude of organisms, particularly in parasites, where several clones are commonly sharing limited resources inside their host. In theory, increased or decreased transmission investment might maximize parasite fitness in the face of competition, but, to our knowledge, this has not been tested experimentally. We developed and used a clone-specific, stage-specific, quantitative PCR protocol to quantify Plasmodium chabaudi replication and transmission stage densities in mixed-clone infections. We co-infected mice from two strains with an avirulent and virulent parasite clone and found competitive suppression of in-host (blood-stage) parasite densities and generally corresponding reductions in transmission stage production, with the virulent clone obtaining overall competitive superiority. In response to competitive suppression, there was little evidence of any alteration in transmission stage investment, apart from a small reduction by one of the two clones in one of the two host strains. This alteration did not result in a competitive advantage, although it might have reduced the disadvantage. This study supports much of the current literature, which predicts that conspecific in-host competition will result in a competitive advantage and positive selection for virulent clones and thus the evolution of higher virulence.
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