English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

Antimalarial drug resistance has historically arisen through convergent  de novo  mutations in  Plasmodium falciparum  parasite populations in Southeast Asia and South America. For the past decade in Southeast Asia, artemisinins, the core component of first-line antimalarial therapies, have experienced delayed parasite clearance associated with several  pfk13  mutations, primarily C580Y. We report that mutant  pfk13  has emerged independently in Guyana, with genome analysis indicating an evolutionary origin distinct from Southeast Asia.  Pfk13  C580Y parasites were observed in 1.6% (14/854) of samples collected in Guyana in 2016–2017. Introducing  pfk13  C580Y or R539T mutations by gene editing into local parasites conferred high levels of  in vitro  artemisinin resistance.  In vitro  growth competition assays revealed a fitness cost associated with these  pfk13  variants, potentially explaining why these resistance alleles have not increased in frequency more quickly in South America. These data place local malaria control efforts at risk in the Guiana Shield.

Local emergence in Amazonia of Plasmodium falciparum k13 C580Y mutants associated with in vitro artemisinin resistance