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Human erythroid progenitors are directly infected by SARS-CoV-2: Implications for emerging erythropoiesis in severe COVID-19 patients.

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journal contribution
posted on 31.03.2021, 11:14 by Hector Huerga Encabo, William Grey, Manuel Garcia-Albornoz, Henry Wood, Rachel Ulferts, Iker Valle Aramburu, Austin G Kulasekararaj, Ghulam Mufti, Venizelos Papayannopoulos, Rupert Beale, Dominique Bonnet
We document here that intensive care COVID-19 patients suffer a profound decline in hemoglobin levels but show an increase of circulating nucleated red cells, suggesting that SARS-CoV-2 infection either directly or indirectly induces stress erythropoiesis. We show that ACE2 expression peaks during erythropoiesis and renders erythroid progenitors vulnerable to infection by SARS-CoV-2. Early erythroid progenitors, defined as CD34-CD117+CD71+CD235a-, show the highest levels of ACE2 and constitute the primary target cell to be infected during erythropoiesis. SARS-CoV-2 causes the expansion of colony formation by erythroid progenitors and can be detected in these cells after 2 weeks of the initial infection. Our findings constitute the first report of SARS-CoV-2 infectivity in erythroid progenitor cells and can contribute to understanding both the clinical symptoms of severe COVID-19 patients and how the virus can spread through the circulation to produce local inflammation in tissues, including the bone marrow.

Funding

Crick (Grant ID: 10827, Grant title: Beale FC001827) Crick (Grant ID: 10045, Grant title: Bonnet FC001045) Crick (Grant ID: 10129, Grant title: Papayannopoulos FC001129)

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