Elizabeth Egan
Stanford University, CA·Microbiology & Immunology
Malaria kills hundreds of thousands of people a year, most of them young children and pregnant women, and control is slipping because there is no highly effective vaccine and the parasite keeps evolving drug resistance. Most severe disease comes from *Plasmodium falciparum*, a parasite that can only survive inside human red blood cells.
- Fields
Microbiology & Immunology
Biology
Medicine & Clinical Research
- Topics
malaria
Plasmodium falciparum
red blood cell
- Grants
- 1 known grant, through Jun 2028
What they work on
- Determine which precise steps of Plasmodium falciparum invasion of human red blood cells require the surface proteins CD44 and CD55, using live-cell imaging and advanced microscopy of CRISPR-edited cultured red blood cells.
- Identify the parasite and red blood cell proteins that bind CD44 and CD55, using avidity-based pulldowns and proximity labeling proteomics that chemically tag a protein's molecular neighbors.
- Define the signaling pathways switched on inside the human red blood cell during parasite invasion and test whether they require CD44 and CD55.
- Apply CRISPR-Cas9 editing of primary human hematopoietic stem cells followed by ex vivo differentiation into mature cultured red blood cells to make these DNA-free host cells genetically tractable for infection studies.
More about the research
That dependence is also an opportunity: if the parasite needs specific human proteins to break into a red blood cell, those human proteins become drug targets that the parasite cannot simply mutate away. The obstacle has been technical — mature red blood cells have no DNA, so the usual genetic tools do not work on them.
Why it matters
New approaches to malaria control are needed as drug resistance spreads and no effective vaccine exists. Pinpointing how the human red blood cell proteins CD44 and CD55 let *Plasmodium falciparum* invade could lay groundwork for host-directed therapies — drugs aimed at the human receptor rather than the parasite, which may be harder for the parasite to evade — and could inform vaccine design targeting the parasite proteins that bind them.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Daniel Goldberg
Washington University in St Louis, MO·Microbiology & Immunology
Define how two new putative allosteric inhibitors of PfNCR1, a malaria parasite cholesterol pump, block its function, combining cryo-EM structures with physiological, genetic and cell biological approaches.
Sudhir Kumar
Iowa State University, IA·Microbiology & Immunology
Determine how the male-specific kinase SRPK1 controls splicing of axoneme gene transcripts in Plasmodium falciparum, using proximity labeling to identify SRPK1-spliceosome complex proteins.
Steve Taylor
Duke University, NC·Microbiology & Immunology
Test whether parasite overexpression of mutant Pfsa3 (PF3D7_1127000), a putative protein phosphatase, nullifies sickle trait's protection, by engineering transgenic Plasmodium falciparum lines expressing wildtype and mutant forms.
The school
Stanford University: 87 labs on PI Pages, $1.6B a year on research, 739 research doctorates a year.
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