Anthony Ruberto
Florida State University, FL·Microbiology & Immunology·Early-career
Malaria still causes an estimated 229 million cases and 409,000 deaths each year. The drugs that work best against the deadliest malaria parasite, Plasmodium falciparum, belong to the artemisinin family, and they are losing ground: in parts of the world, parasites now survive treatment long enough to clear from the blood unusually slowly, a state called partial artemisinin resistance.
- Fields
Microbiology & Immunology
Genetics
Public Health & Epidemiology
- Topics
malaria
Plasmodium falciparum
artemisinin resistance
- Grants
- 1 known grant, through Apr 2028
What they work on
- Determine the genetic changes underlying the cellular and transcriptomic differences between artemisinin-resistant and -sensitive Plasmodium falciparum, using long-read and short-read sequencing plus Chromosome Conformation Capture sequencing to map genome folding.
- Test whether two candidate RNA-binding proteins — regulators that control gene expression after transcription — are required for artemisinin resistance, using inducible knockdown lines and phenotypic drug-survival assays.
- Identify the RNA transcripts bound by each candidate RNA-binding protein using eCLIP-seq, which crosslinks proteins to their RNA partners before sequencing, to reveal the pathways they regulate during drug stress.
- Characterize the transcriptional signatures of resistant versus sensitive ring-stage parasites by single-cell RNA sequencing of lines derived from a Kelch 13 mutant field isolate evolved in vitro.
More about the research
That delay also raises the risk that the partner drugs used alongside artemisinin will fail, opening the door to multi-drug resistant parasites. Most research has centered on mutations in a parasite protein called Kelch 13, which slow the digestion of hemoglobin that the parasite needs in order to activate artemisinin. Those mutations explain part of the picture but not all of it, and the remaining mechanisms are unknown.
Why it matters
Artemisinin combination therapy is the frontline treatment for the deadliest human malaria parasite, and spreading resistance threatens elimination efforts worldwide. Identifying RNA-binding proteins and the transcripts they control as contributors to resistance could supply new molecular markers for tracking resistance in the field and new targets for drugs designed to restore artemisinin's effectiveness.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Jennifer Small-Saunders
Columbia University, NY·Microbiology & Immunology·Early-career
Identify long noncoding RNAs and tRNA-derived fragments that change in artemisinin-resistant versus sensitive Plasmodium falciparum after drug exposure or isoleucine starvation, using transcriptomics.
Jessica Lin
University of North Carolina at Chapel Hill, NC·Microbiology & Immunology
Test whether primaquine failures in a Thai Plasmodium vivax relapse trial were driven by a high burden of hypnozoites, dormant liver-stage parasites, using molecular inversion probe sequencing to detect circulating variants and gauge infection complexity.
Jonathan Juliano
University of North Carolina at Chapel Hill, NC·Microbiology & Immunology·Early-career
Build a temporal deep learning surrogate, a neural network trained on simulation output, to predict how antimalarial drug policy changes would alter resistance and transmission in Kinshasa Province, Democratic Republic of the Congo.
The school
Florida State University: 15 labs on PI Pages, $461M a year on research, 481 research doctorates a year.
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