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RESEARCH PAPER / 2025-03-03

SARS-CoV-2 pseudovirus dysregulates hematopoiesis and induces inflammaging of hematopoietic stem and progenitor cells.

Dong-Hoon Chae, Hyun Sung Park, Kyoung-Myeon Kim, Aaron Yu, Jae Han Park, Mi-Kyung Oh, Soon Won Choi, Jaechul Ryu, Cynthia E Dunbar, Hee Min Yoo, Kyung-Rok Yu

Department of Agricultural Biotechnology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea.Department of Agricultural Biotechnology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea. · pubmed

Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the respiratory system but may induce hematological alterations such as anemia, lymphopenia and thrombocytopenia. Previous studies have reported that SARS-CoV-2 efficiently infects hematopoietic stem and progenitor cells (HSPCs); however, the subsequent effects on hematopoiesis and immune reconstitution have not yet been described. Here we evaluated the pathological effects of infection of umbilical-cord-blood-derived HSPCs with the SARS-CoV-2 Omicron variant pseudovirus (PsV). Transcriptomic analysis of Omicron PsV-infected HSPCs revealed the upregulation of genes involved in inflammation, aging and the NLRP3 inflammasome, suggesting a potential trigger of inflammaging. Omicron PsV-infected HSPCs presented decreased numbers of multipotential progenitors (granulocyte‒erythrocyte‒macrophage‒megakaryocyte colony-forming units) ex vivo and repopulated primitive hematopoietic stem cells (Ki-67

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Research summary

The paper claims that SARS-CoV-2 infection of hematopoietic stem and progenitor cells induces dysregulation of hematopoiesis and triggers inflammaging. This research is relevant as it explores the mechanisms by which viral infection may contribute to aging processes at the cellular level, particularly in hematopoietic cells, which could have implications for understanding age-related decline in immune function.

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