Progression of Plasmodium berghei through Anopheles stephensi Is Density-Dependent

Sinden, Robert E.; Dawes, Emma J; Alavi, Yasmene; Waldock, Joanna; Finney, Olivia; Mendoza, Jacqui; Butcher, G. A.; Andrews, Laura; Hill, Adrian V. S.; Gilbert, Sarah C.; Basáñez, María‐Gloria

doi:10.1371/journal.ppat.0030195

Cited by 123 publications

(141 citation statements)

References 83 publications

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“…To complete their life cycle, parasites must cross GE50CH20-BarillasMury ARI 26 September 2016 11:59 multiple barriers, including the epithelial layers of the midgut and salivary glands, and survive the epithelial defense responses and the systemic antiplasmodial responses mounted by the mosquito immune system (5,13,14,19). This is a difficult and dangerous journey, and the parasite suffers major losses at each developmental step in the mosquito (90). Several environmental, behavioral, cellular, and biochemical factors determine the ability of a mosquito to transmit malaria (i.e., the mosquito's vectorial capacity).…”

Section: Plasmodium Biology In the Mosquito And Vectorial Capacitymentioning

confidence: 99%

Mosquito Vectors and the Globalization of Plasmodium falciparum Malaria

et al. 2016

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Plasmodium falciparum malaria remains a devastating public health problem. Recent discoveries have shed light on the origin and evolution of Plasmodium parasites and their interactions with their vertebrate and mosquito hosts. P. falciparum malaria originated in Africa from a single horizontal transfer between an infected gorilla and a human, and became global as the result of human migration. Today, P. falciparum malaria is transmitted worldwide by more than 70 different anopheline mosquito species. Recent studies indicate that the mosquito immune system can be a barrier to malaria transmission and that the P. falciparum Pfs47 gene allows the parasite to evade mosquito immune detection. Here, we review the origin and globalization of P. falciparum and integrate this history with analysis of the biology, evolution, and dispersal of the main mosquito vectors. This new perspective broadens our understanding of P. falciparum population structure and the dispersal of important parasite genetic traits. 20.1

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Section: Plasmodium Biology In the Mosquito And Vectorial Capacitymentioning

confidence: 99%

Mosquito Vectors and the Globalization of Plasmodium falciparum Malaria

et al. 2016

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“…Evidence is now accumulating that input parasite densities affect the progression of the infection as well as mosquito signaling pathways and mortality; however, the actual impact of infection intensities on mosquito responses is still unclear, and very few studies have considered infection intensities in the analysis of infection data (7,24,26). Here we have carried out A. gambiae infections with geographically related P. falciparum parasites sampled from naturally infected children in order to investigate the impact of different infection intensities on the mosquito midgut transcriptome.…”

Section: Rna Interference (Rnai)-mediated Gene Silencing Provides Inimentioning

confidence: 99%

“…In fact, A. gambiae is not a natural vector of P. berghei, and the intensities of P. berghei infection are much higher than those commonly observed in nature with P. falciparum (2). Differences in P. falciparum infection levels have been associated with several genomic loci and have been shown to depend on vector-parasite genotype-by-genotype interactions (12,16,29).Evidence is now accumulating that input parasite densities affect the progression of the infection as well as mosquito signaling pathways and mortality; however, the actual impact of infection intensities on mosquito responses is still unclear, and very few studies have considered infection intensities in the analysis of infection data (7,24,26). Here we have carried out A. gambiae infections with geographically related P. falciparum parasites sampled from naturally infected children in order to investigate the impact of different infection intensities on the mosquito midgut transcriptome.…”

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confidence: 99%

Infection Intensity-Dependent Responses of Anopheles gambiae to the African Malaria Parasite Plasmodium falciparum

et al. 2011

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Malaria remains a devastating disease despite efforts at control and prevention. Extensive studies using mostly rodent infection models reveal that successful Plasmodium parasite transmission by the African mosquito vector Anopheles gambiae depends on finely tuned vector-parasite interactions. Here we investigate the transcriptional response of A. gambiae to geographically related Plasmodium falciparum populations at various infection intensities and different infection stages. These responses are compared with those of mosquitoes infected with the rodent parasite Plasmodium berghei. We demonstrate that mosquito responses are largely dependent on the intensity of infection. A major transcriptional suppression of genes involved in the regulation of midgut homeostasis is detected in low-intensity P. falciparum infections, the most common type of infection in Africa. Importantly, genes transcriptionally induced during these infections tend to be phylogenetically unique to A. gambiae. These data suggest that coadaptation between vectors and parasites may act to minimize the impact of infection on mosquito fitness by selectively suppressing specific functional classes of genes. RNA interference (RNAi)-mediated gene silencing provides initial evidence for important roles of the mosquito G protein-coupled receptors (GPCRs) in controlling infection intensity-dependent antiparasitic responses.Malaria is a devastating parasitic disease that remains an enormous public health burden, especially in sub-Saharan Africa, where the deadliest of the malaria parasites, Plasmodium falciparum, is transmitted mainly by Anopheles gambiae mosquitoes. Extensive laboratory studies of mosquito-parasite interactions have exploited genomics and postgenomics technologies for gene expression profiling and functional characterization to generate new knowledge. It has been established that parasite development in the mosquito midgut is the most vulnerable stage of the entire transmission cycle. This appears to be due largely to robust mosquito responses that effectively reduce the number of parasites able to invade the midgut and establish infections in the hemolymph (8,22,30). Therefore, detailed understanding of the vector-parasite interactions could lead to novel strategies that can supplement current control methods.Recent studies have identified mosquito genes that affect P. falciparum and the rodent malaria parasite, Plasmodium berghei, which is often used as a laboratory model, similarly; however, such conserved responses can only partly explain the vector-parasite interactions in natural settings (6,8,11,20,21). In fact, A. gambiae is not a natural vector of P. berghei, and the intensities of P. berghei infection are much higher than those commonly observed in nature with P. falciparum (2). Differences in P. falciparum infection levels have been associated with several genomic loci and have been shown to depend on vector-parasite genotype-by-genotype interactions (12,16,29).Evidence is now accumulating that input parasite densities affe...

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“…31 Transmission from a vertebrate to an invertebrate host and back are arguably the most critical events in the pathogen life cycle, as reflected by dramatic population bottlenecks. 50,51 In order to establish an infection in the new host the malarial parasite forms tailor-made extracellular stages that display the above-mentioned gliding motility. Hsp20(-) parasites displayed reduced ookinete motility, that is parasites formed in the blood bolus inside the mosquito midgut move substantially slower in the absence of Hsp20.…”

Section: Cell Migration Of Malaria Parasitesmentioning

confidence: 99%