Article Synopsis
- Intensive care COVID-19 patients experience a significant drop in hemoglobin levels but an increase in nucleated red blood cells, indicating the virus may trigger stress-related blood cell production.
- The study identifies that ACE2, which peaks during blood cell production, makes early erythroid progenitors (specific stem cells that develop into red blood cells) particularly susceptible to SARS-CoV-2 infection.
- Findings reveal that SARS-CoV-2 can infect these progenitor cells, contributing to understanding severe COVID-19 symptoms and the virus's potential to spread and cause local inflammation in various tissues, including the bone marrow.
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Article 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 CD34CD117CD71CD235a, 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7862909 | PMC |
| http://dx.doi.org/10.1016/j.stemcr.2021.02.001 | DOI Listing |
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