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Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies

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Resumo:Antimalarial chemotherapy, globally reliant on artemisinin-based combination therapies (ACTs), is threatened by the spread of drug resistance in Plasmodium falciparum parasites. Here we use zinc-finger nucleases to genetically modify the multidrug resistance-1 transporter PfMDR1 at amino acids 86 and 184, and demonstrate that the widely prevalent N86Y mutation augments resistance to the ACT partner drug amodiaquine and the former first-line agent chloroquine. In contrast, N86Y increases parasite susceptibility to the partner drugs lumefantrine and mefloquine, and the active artemisinin metabolite dihydroartemisinin. The PfMDR1 N86 plus Y184F isoform moderately reduces piperaquine potency in strains expressing an Asian/African variant of the chloroquine resistance transporter PfCRT. Mutations in both digestive vacuole-resident transporters are thought to differentially regulate ACT drug interactions with host haem, a product of parasite-mediated haemoglobin degradation. Global mapping of these mutations illustrates where the different ACTs could be selectively deployed to optimize treatment based on regional differences in PfMDR1 haplotypes.
Autores principais:Veiga, Maria Isabel Mendes
Outros Autores:Dhingra, Satish K.; Henrich, Philipp P.; Straimer, Judith; Gnädig, Nina; Uhlemann, Anne-Catrin; Martin, Rowena E.; Lehane, Adele M.; Fidock, David A.
Assunto:Ciências Médicas::Medicina Básica
Ano:2016
País:Portugal
Tipo de documento:artigo
Tipo de acesso:acesso aberto
Instituição associada:Universidade do Minho
Idioma:inglês
Origem:RepositóriUM - Universidade do Minho
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author Veiga, Maria Isabel Mendes
author2 Dhingra, Satish K.
Henrich, Philipp P.
Straimer, Judith
Gnädig, Nina
Uhlemann, Anne-Catrin
Martin, Rowena E.
Lehane, Adele M.
Fidock, David A.
author2_role author
author
author
author
author
author
author
author
author_facet Veiga, Maria Isabel Mendes
Dhingra, Satish K.
Henrich, Philipp P.
Straimer, Judith
Gnädig, Nina
Uhlemann, Anne-Catrin
Martin, Rowena E.
Lehane, Adele M.
Fidock, David A.
author_role author
contributor_name_str_mv RepositóriUM - Universidade do Minho
country_str PT
creators_json_txt [{\"Person.name\":\"Veiga, Maria Isabel Mendes\"},{\"Person.name\":\"Dhingra, Satish K.\"},{\"Person.name\":\"Henrich, Philipp P.\"},{\"Person.name\":\"Straimer, Judith\"},{\"Person.name\":\"Gnädig, Nina\"},{\"Person.name\":\"Uhlemann, Anne-Catrin\"},{\"Person.name\":\"Martin, Rowena E.\"},{\"Person.name\":\"Lehane, Adele M.\"},{\"Person.name\":\"Fidock, David A.\"}]
datacite.contributors.contributor.contributorName.fl_str_mv RepositóriUM - Universidade do Minho
datacite.creators.creator.creatorName.fl_str_mv Veiga, Maria Isabel Mendes
Dhingra, Satish K.
Henrich, Philipp P.
Straimer, Judith
Gnädig, Nina
Uhlemann, Anne-Catrin
Martin, Rowena E.
Lehane, Adele M.
Fidock, David A.
datacite.date.Accepted.fl_str_mv 2016-05-01T00:00:00Z
datacite.date.available.fl_str_mv 2017-04-12T16:41:06Z
datacite.date.embargoed.fl_str_mv 2017-04-12T16:41:06Z
datacite.rights.fl_str_mv http://purl.org/coar/access_right/c_abf2
datacite.subjects.subject.fl_str_mv Ciências Médicas::Medicina Básica
datacite.titles.title.fl_str_mv Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
dc.contributor.none.fl_str_mv RepositóriUM - Universidade do Minho
dc.creator.none.fl_str_mv Veiga, Maria Isabel Mendes
Dhingra, Satish K.
Henrich, Philipp P.
Straimer, Judith
Gnädig, Nina
Uhlemann, Anne-Catrin
Martin, Rowena E.
Lehane, Adele M.
Fidock, David A.
dc.date.Accepted.fl_str_mv 2016-05-01T00:00:00Z
dc.date.available.fl_str_mv 2017-04-12T16:41:06Z
dc.date.embargoed.fl_str_mv 2017-04-12T16:41:06Z
dc.format.none.fl_str_mv application/pdf
dc.identifier.none.fl_str_mv https://hdl.handle.net/1822/45325
dc.language.none.fl_str_mv eng
dc.publisher.none.fl_str_mv Nature Publishing Group
dc.rights.none.fl_str_mv http://purl.org/coar/access_right/c_abf2
dc.subject.none.fl_str_mv Ciências Médicas::Medicina Básica
dc.title.fl_str_mv Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
dc.type.none.fl_str_mv http://purl.org/coar/resource_type/c_6501
description Antimalarial chemotherapy, globally reliant on artemisinin-based combination therapies (ACTs), is threatened by the spread of drug resistance in Plasmodium falciparum parasites. Here we use zinc-finger nucleases to genetically modify the multidrug resistance-1 transporter PfMDR1 at amino acids 86 and 184, and demonstrate that the widely prevalent N86Y mutation augments resistance to the ACT partner drug amodiaquine and the former first-line agent chloroquine. In contrast, N86Y increases parasite susceptibility to the partner drugs lumefantrine and mefloquine, and the active artemisinin metabolite dihydroartemisinin. The PfMDR1 N86 plus Y184F isoform moderately reduces piperaquine potency in strains expressing an Asian/African variant of the chloroquine resistance transporter PfCRT. Mutations in both digestive vacuole-resident transporters are thought to differentially regulate ACT drug interactions with host haem, a product of parasite-mediated haemoglobin degradation. Global mapping of these mutations illustrates where the different ACTs could be selectively deployed to optimize treatment based on regional differences in PfMDR1 haplotypes.
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eu_rights_str_mv openAccess
format article
fulltext.url.fl_str_mv https://repositorium.uminho.pt/bitstreams/3d9bb7fb-6dd0-46f9-b717-7e8d02f95f45/download
id rum_3db92d575669e75b411ae90f2fda4e14
identifier.url.fl_str_mv https://hdl.handle.net/1822/45325
instacron_str repositorium
institution Universidade do Minho
instname_str Universidade do Minho
language eng
network_acronym_str rum
network_name_str RepositóriUM - Universidade do Minho
oai_identifier_str oai:repositorium.uminho.pt:1822/45325
organization_str_mv urn:organizationAcronym:repositorium
person_str_mv Veiga, Maria Isabel Mendes
Dhingra, Satish K.
Henrich, Philipp P.
Straimer, Judith
Gnädig, Nina
Uhlemann, Anne-Catrin
Martin, Rowena E.
Lehane, Adele M.
Fidock, David A.
publishDate 2016
publisher.none.fl_str_mv Nature Publishing Group
reponame_str RepositóriUM - Universidade do Minho
repository_id_str urn:repositoryAcronym:rum
service_str_mv urn:repositoryAcronym:rum
spelling engNature Publishing GroupporAntimalarial chemotherapy, globally reliant on artemisinin-based combination therapies (ACTs), is threatened by the spread of drug resistance in Plasmodium falciparum parasites. Here we use zinc-finger nucleases to genetically modify the multidrug resistance-1 transporter PfMDR1 at amino acids 86 and 184, and demonstrate that the widely prevalent N86Y mutation augments resistance to the ACT partner drug amodiaquine and the former first-line agent chloroquine. In contrast, N86Y increases parasite susceptibility to the partner drugs lumefantrine and mefloquine, and the active artemisinin metabolite dihydroartemisinin. The PfMDR1 N86 plus Y184F isoform moderately reduces piperaquine potency in strains expressing an Asian/African variant of the chloroquine resistance transporter PfCRT. Mutations in both digestive vacuole-resident transporters are thought to differentially regulate ACT drug interactions with host haem, a product of parasite-mediated haemoglobin degradation. Global mapping of these mutations illustrates where the different ACTs could be selectively deployed to optimize treatment based on regional differences in PfMDR1 haplotypes.application/pdfporGlobally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapiesVeiga, Maria Isabel MendesDhingra, Satish K.Henrich, Philipp P.Straimer, JudithGnädig, NinaUhlemann, Anne-CatrinMartin, Rowena E.Lehane, Adele M.Fidock, David A.HostingInstitutionOrganizationalRepositóriUM - Universidade do Minhoe-mailmailto:repositorium@usdb.uminho.ptrepositorium@usdb.uminho.ptCITATIONVeiga, M. I., Dhingra, S. K., Henrich, P. P., Straimer, J., Gnädig, N., Uhlemann, A. C., . . . Fidock, D. A. (2016). Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies. Nature Communications, 7. doi: 10.1038/ncomms11553PMID27189525ISSNIsPartOf2041-1723DOIIsPartOf10.1038/ncomms115532017-04-12T16:41:06Z2016-052015-102017-02-13T13:01:01Z2016-05-01T00:00:00ZHandlehttps://hdl.handle.net/1822/45325http://purl.org/coar/access_right/c_abf2open accesshttp://www.oecd.org/science/inno/38235147.pdfFields of Science and Technology (FOS)Ciências Médicas::Medicina Básica1379153 bytesliteraturehttp://purl.org/coar/resource_type/c_6501journal articlehttp://purl.org/coar/access_right/c_abf2application/pdffulltexthttps://repositorium.uminho.pt/bitstreams/3d9bb7fb-6dd0-46f9-b717-7e8d02f95f45/download
spellingShingle Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
Veiga, Maria Isabel Mendes
Ciências Médicas::Medicina Básica
status SINGLETON
subject.other.fl_str_mv Ciências Médicas::Medicina Básica
title Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
title_full Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
title_fullStr Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
title_full_unstemmed Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
title_short Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
title_sort Globally prevalent PfMDR1 mutations modulate Plasmodium falciparum susceptibility to artemisinin-based combination therapies
topic Ciências Médicas::Medicina Básica
topic_facet Ciências Médicas::Medicina Básica
url https://hdl.handle.net/1822/45325
visible 1