ArticleBlood advances2023
Elucidating parasite and host-cell factors enabling Babesia infection in sickle red cells under hypoxic/hyperoxic conditions.
Article in Blood advances, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- More than malaria: ExploringCurrent research in parasitology & vector-borne diseases · 2026Review
- Shared host, distinct invaders: metabolomic footprints of plasmodium and babesia in host red cells.Current opinion in hematology · 2025Review
- Article
- Article
- Identification and characterization of extracellular vesicles from red cells infected withFrontiers in cellular and infection microbiology · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Sickle red blood cells (RBCs) represent a naturally existing host-cell resistance mechanism to hemoparasite infections. We investigate the basis of this resistance using Babesia divergens grown in sickle (SS) and sickle trait (AS) cells. We found that oxygenation and its corresponding effect on RBC sickling, frequency of fetal hemoglobin positive (HbF+) cells, cellular redox environment, and parasite proliferation dynamics, all played a role in supporting or inhibiting Babesia proliferation. To identify cellular determinants that supported infection, an image flow cytometric tool was developed that could identify sickled cells and constituent Hb. We showed that hypoxic conditions impaired parasite growth in both SS and AS cells. Furthermore, cell sickling was alleviated by oxygenation (hyperoxic conditions), which decreased inhibition of parasite proliferation in SS cells. Interestingly, our tool identified HbF+-SS as host-cells of choice under both hypoxic and hyperoxic conditions, which was confirmed using cord RBCs containing high amounts of HbF+ cells. Uninfected SS cells showed a higher reactive oxygen species-containing environment, than AA or AS cells, which was further perturbed on infection. In hostile SS cells we found that Babesia alters its subpopulation structure, with 1N dominance under hypoxic conditions yielding to equivalent ratios of all parasite forms at hyperoxic conditions, favorable for growth. Multiple factors, including oxygenation and its impact on cell shape, HbF positivity, redox status, and parasite pleiotropy allow Babesia propagation in sickle RBCs. Our studies provide a cellular and molecular basis of natural resistance to Babesia, which will aid in defining novel therapies against human babesiosis.
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