{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T19:45:42Z","timestamp":1792093542795,"version":"4.4.0"},"reference-count":86,"publisher":"MDPI AG","issue":"3","license":[{"start":{"date-parts":[[2025,1,21]],"date-time":"2025-01-21T00:00:00Z","timestamp":1737417600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19, a respiratory disease that can range in presentation from mild symptoms to severe conditions such as pneumonia and acute respiratory distress syndrome. SARS-CoV-2, a single-stranded RNA virus, spreads through aerosols and respiratory droplets. It enters human cells by binding to the angiotensin-converting enzyme 2 receptor, leading to various complications, including significant alterations in red blood cells and potential disruptions in haemoglobin function and oxygen transport. During infection, the interaction between hypoxia, inflammation, and haematopoiesis affects erythropoiesis at multiple levels. Hypoxia and inflammation, resulting from lung complications and a reduced red blood cell count, influence the regulation of hepcidin, a key regulator of iron levels in the blood. Elevated hepcidin levels are associated with hypoxia and the suppression of erythroferrone, a hormone that normally inhibits hepcidin production. Despite high levels of inflammation, patients in intensive care units often exhibit elevated ferritin levels, which, rather than indicating low hepcidin, suggest disrupted iron metabolism and the development of severe anaemia. Iron is kept in stores, likely due to paradoxically high hepcidin levels, which explains the elevated ferritin measurements. An increase in immature blood cells and a decrease in CD71+ erythroid cells are observed. The elevated levels of CD71+ erythroid cells highlight their dual role in modulating hyper-inflammation and immune response during disease progression. This review examines the pathway by which SARS-CoV-2 affects red blood cell production and the haematopoietic system and how it triggers cytokine storms through interleukins, immature blood cells, and CD71+ erythroid cells. Understanding these processes provides novel pathways for managing haematological manifestations and immune responses in patients with COVID-19.<\/jats:p>","DOI":"10.3390\/ijms26030874","type":"journal-article","created":{"date-parts":[[2025,1,21]],"date-time":"2025-01-21T06:53:32Z","timestamp":1737442412000},"page":"874","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Haematological Manifestations of SARS-CoV-2: Insights into Erythropoiesis, Hepcidin Regulation, and Cytokine Storm"],"prefix":"10.3390","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0009-0001-8541-0951","authenticated-orcid":false,"given":"Elahi","family":"Parham","sequence":"first","affiliation":[{"name":"Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makky","family":"Ahmad","sequence":"additional","affiliation":[{"name":"Department of Medicine and Surgery, University of Pavia, 27100 Pavia, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9801-7235","authenticated-orcid":false,"given":"Marco","family":"Falasca","sequence":"additional","affiliation":[{"name":"Department of Medicine and Surgery, University of Parma, 43125 Parma, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,1,21]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"270","DOI":"10.1038\/s41579-022-00713-0","article-title":"SARS-CoV-2 pathogenesis","volume":"20","author":"Lamers","year":"2022","journal-title":"Nat. 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