| Literature DB >> 33581053 |
Hector Huerga Encabo1, William Grey1, Manuel Garcia-Albornoz1, Henry Wood2, Rachel Ulferts3, Iker Valle Aramburu4, Austin G Kulasekararaj5, Ghulam Mufti5, Venizelos Papayannopoulos4, Rupert Beale3, Dominique Bonnet6.
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.Entities:
Keywords: SARS-CoV-2; anemia; erythropoiesis; human hematopoietic stem/progenitor cells; hypoxia
Year: 2021 PMID: 33581053 PMCID: PMC7862909 DOI: 10.1016/j.stemcr.2021.02.001
Source DB: PubMed Journal: Stem Cell Reports ISSN: 2213-6711 Impact factor: 7.765