Emmanuel Bischoff

Publications (25) View all

• Article: Evidence for Population-Specific Positive Selection on Immune Genes of Anopheles gambiae.

  Jacob E Crawford, Emmanuel Bischoff, Thierry Garnier, Awa Gneme, Karin Eiglmeier, Inge Holm, Michelle M Riehle, Wamdaogo M Guelbeogo, N'fale Sagnon, Brian P Lazzaro, Kenneth D Vernick
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  ABSTRACT: Host-pathogen interactions can be powerful drivers of adaptive evolution, shaping the patterns of molecular variation at the genes involved. In this study, we sequenced alleles from 28 immune-related loci in wild samples of multiple genetic subpopulations of the African malaria mosquito Anopheles gambiae, obtaining unprecedented sample sizes and providing the first opportunity to contrast patterns of molecular evolution at immune-related loci in the recently discovered GOUNDRY population to those of the indoor-resting M and S molecular forms. In contrast to previous studies that focused on immune genes identified in laboratory studies, we centered our analysis on genes that fall within a quantitative trait locus associated with resistance to Plasmodium falciparum in natural populations of A. gambiae. Analyses of haplotypic and genetic diversity at these 28 loci revealed striking differences among populations in levels of genetic diversity and allele frequencies in coding sequence. Putative signals of positive selection were identified at 11 loci, but only one was shared by two subgroups of A. gambiae. Striking patterns of linkage disequilibrium were observed at several loci. We discuss these results with respect to ecological differences among these strata as well as potential implications for disease transmission.
  G3 (Bethesda, Md.). 12/2012; 2(12):1505-19.
• Article: Validation of BdCCp2 as a marker for Babesia divergens sexual stages in ticks.

  Claire A M Becker, Laurence Malandrin, Thibaut Larcher, Alain Chauvin, Emmanuel Bischoff, Sarah I Bonnet
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  ABSTRACT: Babesiosis is a tick-transmitted disease of mammalian hosts, caused by the intraerythrocytic protozoan parasites of the genus Babesia. Transmission of Babesia parasites from the vertebrate host to the tick is mediated by sexual stages, the gametocytes which are the only intraerythrocytic stages that survive and develop inside the vector. Very few data are available concerning these parasite stages and some markers are needed in order to refine our knowledge of Babesia life cycle inside the tick and to permit the monitoring of parasite transmission from vertebrate to vector. We previously identified some potential markers of the Babesia divergens gametocytes using an in silico post-genomic approach based on sequence identity between the available genomes of Plasmodium and Babesia spp. Here, one of the identified proteins, BdCCp2, was validated as a marker of sexual stages of B. divergens, in infected ticks challenged with antisera directed against recombinant BdCCp2 protein. The BdCCp2 protein was detected by Western blot in some infected ticks, as a discrete band of approximately 171 kDa, while no signal was detected in the laboratory-reared non-infected tick. BdCCp2 was also detected, by immunohistochemical analyses, in piriform or ovoid bodies, measuring 2.5 to 4.5 μm in diameter, in the gut of partially engorged ticks that were experimentally infected. This molecular marker can then be used in the future to characterize and analyze the biology of B. divergens gametocytes.
  Experimental Parasitology 10/2012; · 2.12 Impact Factor
• Article: A switch in infected erythrocyte deformability at the maturation and blood circulation of Plasmodium falciparum transmission stages.

  Marta Tibúrcio, Makhtar Niang, Guillaume Deplaine, Sylvie Perrot, Emmanuel Bischoff, Papa Alioune Ndour, Francesco Silvestrini, Ayman Khattab, Geneviève Milon, Peter H David, Max Hardeman, Kenneth D Vernick, Robert W Sauerwein, Peter R Preiser, Odile Mercereau-Puijalon, Pierre Buffet, Pietro Alano, Catherine Lavazec
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  ABSTRACT: Achievement of malaria elimination requires development of novel strategies interfering with parasite transmission, including targeting the parasite sexual stages (gametocytes). The formation of Plasmodium falciparum gametocytes in the human host takes several days during which immature gametocyte-infected erythrocytes (GIEs) sequester in host tissues. Only mature stage GIEs circulate in the peripheral blood, available to uptake by the Anopheles vector. Mechanisms underlying GIE sequestration and release in circulation are virtually unknown. We show here that mature GIEs are more deformable than immature stages using ektacytometry and microsphiltration methods, and that a switch in cellular deformability in the transition from immature to mature gametocytes is accompanied by the deassociation of parasite-derived STEVOR proteins from the infected erythrocyte membrane. We hypothesize that mechanical retention contributes to sequestration of immature GIEs and that regained deformability of mature gametocytes is associated with their release in the bloodstream and ability to circulate. These processes are proposed to play a key role in P falciparum gametocyte development in the host and to represent novel and unconventional targets for interfering with parasite transmission.
  Blood 04/2012; 119(24):e172-80. · 9.90 Impact Factor
• Source

  Available from: Catherine Bourgouin

  Article: Diverged Alleles of the Anopheles gambiae Leucine-Rich Repeat Gene APL1A Display Distinct Protective Profiles against Plasmodium falciparum.

  Inge Holm, Catherine Lavazec, Thierry Garnier, Christian Mitri, Michelle M Riehle, Emmanuel Bischoff, Emma Brito-Fravallo, Eizo Takashima, Isabelle Thiery, Agnes Zettor, Stephane Petres, Catherine Bourgouin, Kenneth D Vernick, Karin Eiglmeier
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  ABSTRACT: Functional studies have demonstrated a role for the Anopheles gambiae APL1A gene in resistance against the human malaria parasite, Plasmodium falciparum. Here, we exhaustively characterize the structure of the APL1 locus and show that three structurally different APL1A alleles segregate in the Ngousso colony. Genetic association combined with RNAi-mediated gene silencing revealed that APL1A alleles display distinct protective profiles against P. falciparum. One APL1A allele is sufficient to explain the protective phenotype of APL1A observed in silencing experiments. Epitope-tagged APL1A isoforms expressed in an in vitro hemocyte-like cell system showed that under assay conditions, the most protective APL1A isoform (APL1A(2)) localizes within large cytoplasmic vesicles, is not constitutively secreted, and forms only one protein complex, while a less protective isoform (APL1A(1)) is constitutively secreted in at least two protein complexes. The tested alleles are identical to natural variants in the wild A. gambiae population, suggesting that APL1A genetic variation could be a factor underlying natural heterogeneity of vector susceptibility to P. falciparum.
  PLoS ONE 01/2012; 7(12):e52684. · 4.09 Impact Factor
• Source

  Available from: Innocent Safeukui

  Article: Plasmodium falciparum STEVOR proteins impact erythrocyte mechanical properties.

  Sohini Sanyal, Stéphane Egée, Guillaume Bouyer, Sylvie Perrot, Innocent Safeukui, Emmanuel Bischoff, Pierre Buffet, Kirk W Deitsch, Odile Mercereau-Puijalon, Peter H David, Thomas J Templeton, Catherine Lavazec
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  ABSTRACT: Infection of erythrocytes with the human malaria parasite, Plasmodium falciparum, results in dramatic changes to the host cell structure and morphology. The predicted functional localization of the STEVOR proteins at the erythrocyte surface suggests that they may be involved in parasite-induced modifications of the erythrocyte membrane during parasite development. To address the biologic function of STEVOR proteins, we subjected a panel of stevor transgenic parasites and wild-type clonal lines exhibiting different expression levels for stevor genes to functional assays exploring parasite-induced modifications of the erythrocyte membrane. Using this approach, we show that stevor expression impacts deformability of the erythrocyte membrane. This process may facilitate parasite sequestration in deep tissue vasculature.
  Blood 11/2011; 119(2):e1-8. · 9.90 Impact Factor