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   <dc:title>Whole genome sequencing to evaluate the resistance landscape&#xd;
                following antimalarial treatment failure with&#xd;
                fosmidomycin-clindamycin</dc:title>
   <dc:creator>Guggisberg, Ann M.</dc:creator>
   <dc:creator>Sundararaman, Sesh A.</dc:creator>
   <dc:creator>Lanaspa, Miguel</dc:creator>
   <dc:creator>Moraleda Redecilla, Cinta</dc:creator>
   <dc:creator>González, Raquel</dc:creator>
   <dc:creator>Mayor Aparicio, Alfredo Gabriel</dc:creator>
   <dc:creator>Cisteró, Pau</dc:creator>
   <dc:creator>Hutchinson, David</dc:creator>
   <dc:creator>Kremsner, Peter G.</dc:creator>
   <dc:creator>Hahn, Beatrice H.</dc:creator>
   <dc:creator>Bassat Orellana, Quique</dc:creator>
   <dc:creator>Odom, Audrey R.</dc:creator>
   <dc:subject>Malària</dc:subject>
   <dc:subject>Plasmodium falciparum</dc:subject>
   <dc:subject>Vacuna de la malària</dc:subject>
   <dc:subject>Malaria</dc:subject>
   <dc:subject>Plasmodium falciparum</dc:subject>
   <dc:subject>Malaria vaccine</dc:subject>
   <dcterms:abstract>Novel antimalarial therapies are needed in the face of emerging&#xd;
                resistance to artemisinin combination therapies. A previous&#xd;
                study found a high cure rate in Mozambican children with&#xd;
                uncomplicated Plasmodium falciparum malaria 7 days post&#xd;
                treatment with a fosmidomycin-clindamycin combination. However,&#xd;
                28-day cure rates were low (45.9%), due to parasite&#xd;
                recrudescence. We sought to identify any genetic changes&#xd;
                underlying parasite recrudescence. To this end, we utilized a&#xd;
                selective whole genome amplification method to amplify parasite&#xd;
                genomes from blood spot DNA samples. Parasite genomes from&#xd;
                pre-treatment and post-recrudescence samples were subjected to&#xd;
                whole genome sequencing to identify nucleotide variants. We find&#xd;
                that our data do not support the existence of a genetic change&#xd;
                responsible for recrudescence following fosmidomycin-clindamycin&#xd;
                treatment. Additionally, we find that previously described&#xd;
                resistance alleles for these drugs do not represent biomarkers&#xd;
                of recrudescence. Future studies should continue to optimize&#xd;
                fosmidomycin combinations for use as antimalarial therapies.</dcterms:abstract>
   <dcterms:issued>2016-09-05T12:52:52Z</dcterms:issued>
   <dcterms:issued>2017-07-20T22:01:24Z</dcterms:issued>
   <dcterms:issued>2016-07-20</dcterms:issued>
   <dcterms:issued>2016-08-03T18:01:09Z</dcterms:issued>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:type>info:eu-repo/semantics/acceptedVersion</dc:type>
   <dc:relation>Versió postprint del document publicat a:&#xd;
                http://dx.doi.org/10.1093/infdis/jiw304</dc:relation>
   <dc:relation>The Journal of Infectious Diseases, 2016,</dc:relation>
   <dc:relation>http://dx.doi.org/10.1093/infdis/jiw304</dc:relation>
   <dc:rights>(c) Guggisberg et al., 2016</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:publisher>Oxford University Press</dc:publisher>
   <dc:source>Articles publicats en revistes (ISGlobal)</dc:source>
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