Modulation of PF10_0355 (MSPDBL2) Alters Plasmodium falciparum Response to Antimalarial Drugs

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Published inAntimicrobial Agents and Chemotherapy Vol. 57; no. 7; pp. 2937 - 2941
Main Authors VAN TYNE, Daria, UBOLDI, Alessandro D, HEALER, Julie, COWMAN, Alan F, WIRTH, Dyann F
Format Journal Article
LanguageEnglish
Published Washington, DC American Society for Microbiology 01.07.2013
Subjects
Antibiotics. Antiinfectious agents. Antiparasitic agents
Antimalarials
Antimalarials - pharmacology
Base Sequence
Biological and medical sciences
DNA Copy Number Variations
Drug Resistance
Drug Resistance - genetics
Ethanolamines - pharmacology
Fluorenes - pharmacology
Gene Dosage
Gene Frequency
Genes, Protozoan
Malaria, Falciparum
Malaria, Falciparum - drug therapy
Malaria, Falciparum - parasitology
Mechanisms of Resistance
Medical sciences
Mefloquine - pharmacology
Mutation
Parasitic Sensitivity Tests
Pharmacology. Drug treatments
Phenanthrenes - pharmacology
Plasmodium falciparum
Plasmodium falciparum - drug effects
Plasmodium falciparum - genetics
Polymorphism, Single Nucleotide
Protozoan Proteins
Protozoan Proteins - genetics
Sequence Analysis, DNA
Drug
Protozoa
Antimalarial
Plasmodium falciparum
Apicomplexa
Modulation
Parasiticide
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Malaria's ability to rapidly adapt to new drugs has allowed it to remain one of the most devastating infectious diseases of humans. Understanding and tracking the genetic basis of these adaptations are critical to the success of treatment and intervention strategies. The novel antimalarial resistance locus PF10_0355 (Pfmspdbl2) was previously associated with the parasite response to halofantrine, and functional validation confirmed that overexpression of this gene lowered parasite sensitivity to both halofantrine and the structurally related antimalarials mefloquine and lumefantrine, predominantly through copy number variation. Here we further characterize the role of Pfmspdbl2 in mediating the antimalarial drug response of Plasmodium falciparum. Knockout of Pfmspdbl2 increased parasite sensitivity to halofantrine, mefloquine, and lumefantrine but not to unrelated antimalarials, further suggesting that this gene mediates the parasite response to a specific class of antimalarial drugs. A single nucleotide polymorphism encoding a C591S mutation within Pfmspdbl2 had the strongest association with halofantrine sensitivity and showed a high derived allele frequency among Senegalese parasites. Transgenic parasites expressing the ancestral Pfmspdbl2 allele were more sensitive to halofantrine and structurally related antimalarials than were parasites expressing the derived allele, revealing an allele-specific effect on drug sensitivity in the absence of copy number effects. Finally, growth competition experiments showed that under drug pressure, parasites expressing the derived allele of Pfmspdbl2 outcompeted parasites expressing the ancestral allele within a few generations. Together, these experiments demonstrate that modulation of Pfmspdbl2 affects malaria parasite responses to antimalarial drugs.
Malaria's ability to rapidly adapt to new drugs has allowed it to remain one of the most devastating infectious diseases of humans. Understanding and tracking the genetic basis of these adaptations are critical to the success of treatment and intervention strategies. The novel antimalarial resistance locus PF10 _ 0355 ( Pfmspdbl2 ) was previously associated with the parasite response to halofantrine, and functional validation confirmed that overexpression of this gene lowered parasite sensitivity to both halofantrine and the structurally related antimalarials mefloquine and lumefantrine, predominantly through copy number variation. Here we further characterize the role of Pfmspdbl2 in mediating the antimalarial drug response of Plasmodium falciparum . Knockout of Pfmspdbl2 increased parasite sensitivity to halofantrine, mefloquine, and lumefantrine but not to unrelated antimalarials, further suggesting that this gene mediates the parasite response to a specific class of antimalarial drugs. A single nucleotide polymorphism encoding a C591S mutation within Pfmspdbl2 had the strongest association with halofantrine sensitivity and showed a high derived allele frequency among Senegalese parasites. Transgenic parasites expressing the ancestral Pfmspdbl2 allele were more sensitive to halofantrine and structurally related antimalarials than were parasites expressing the derived allele, revealing an allele-specific effect on drug sensitivity in the absence of copy number effects. Finally, growth competition experiments showed that under drug pressure, parasites expressing the derived allele of Pfmspdbl2 outcompeted parasites expressing the ancestral allele within a few generations. Together, these experiments demonstrate that modulation of Pfmspdbl2 affects malaria parasite responses to antimalarial drugs.
Author Dyann F. Wirth
Alessandro D. Uboldi
Alan F. Cowman
Julie Healer
Daria Van Tyne
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Copyright © 2013, American Society for Microbiology. All Rights Reserved.
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Malaria's ability to rapidly adapt to new drugs has allowed it to remain one of the most devastating infectious diseases of humans. Understanding and tracking...
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StartPage 2937
SubjectTerms Antibiotics. Antiinfectious agents. Antiparasitic agents
Antimalarials
Antimalarials - pharmacology
Base Sequence
Biological and medical sciences
DNA Copy Number Variations
Drug Resistance
Drug Resistance - genetics
Ethanolamines - pharmacology
Fluorenes - pharmacology
Gene Dosage
Gene Frequency
Genes, Protozoan
Malaria, Falciparum
Malaria, Falciparum - drug therapy
Malaria, Falciparum - parasitology
Mechanisms of Resistance
Medical sciences
Mefloquine - pharmacology
Mutation
Parasitic Sensitivity Tests
Pharmacology. Drug treatments
Phenanthrenes - pharmacology
Plasmodium falciparum
Plasmodium falciparum - drug effects
Plasmodium falciparum - genetics
Polymorphism, Single Nucleotide
Protozoan Proteins
Protozoan Proteins - genetics
Sequence Analysis, DNA
Title Modulation of PF10_0355 (MSPDBL2) Alters Plasmodium falciparum Response to Antimalarial Drugs
URI http://aac.asm.org/content/57/7/2937.abstract
https://www.ncbi.nlm.nih.gov/pubmed/23587962
https://journals.asm.org/doi/10.1128/AAC.02574-12
https://search.proquest.com/docview/1367879382
https://search.proquest.com/docview/1419368000
https://pubmed.ncbi.nlm.nih.gov/PMC3697352
Volume 57
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