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Human erythroid progenitors are directly infected by SARS-CoV-2: Implications for hypoxia and emerging haematopoiesis/erythropoiesis in COVID-19

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Author(s)

  • Hector Huerga Encabo
  • William George Grey
  • Manuel Garcia-Albornoz
  • Henry Wood
  • Rachel Ulferts
  • Iker Valle Aramburu
  • Austin G Kulasekararaj
  • Ghulam Mufti
  • Venizelos Papayannopoulos
  • Rupert Beale
  • Dominique Bonnet

Department/unit(s)

Publication details

JournalStem Cell Reports
DateAccepted/In press - 1 Feb 2021
DateE-pub ahead of print - 5 Feb 2021
DatePublished (current) - 9 Mar 2021
Issue number3
Volume16
Number of pages8
Pages (from-to)428-436
Early online date5/02/21
Original languageEnglish

Abstract

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.

Bibliographical note

© 2021 The Author(s).

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