ArticlePloS one2026
Omicron SARS-CoV-2 shows NRP1-linked susceptibility in adipose-derived MSCs and alters primitive cord blood CD34⁺ HSPCs.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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20 authors.
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Abstract
SARS-CoV-2 infection is linked to hematologic abnormalities, but whether early hematopoietic compartments and their stromal niche are directly engaged remains unclear. We used in vitro exposure models to compare variant-associated responses of adult mesenchymal stromal cells (MSCs) and umbilical cord blood (UCB) CD34 ⁺ hematopoietic stem and progenitor cells (HSPCs). Adipose-derived (AD) and bone marrow-derived (BM) MSCs exposed to wild-type, Delta, or Omicron showed source- and variant-dependent nucleocapsid protein (NP) positivity, highest with Omicron in AD-MSCs; infectious virus in supernatants was undetectable. AD-MSCs expressed higher neuropilin-1 (NRP1) than BM-MSCs, and NRP1 knockdown reduced Omicron-associated NP signal, implicating an NRP1-linked entry process. SARS-CoV-2 exposure induced indoleamine-2,3-dioxygenase 1 (IDO1), most prominently in AD-MSCs. In UCB CD34 ⁺ HSPCs, Omicron increased NP positivity enriched in long-term HSCs, reduced primitive fraction frequencies, increased colony formation, and promoted early erythroid progenitor accumulation; heat-inactivated virus did not. NanoString profiling revealed host-response activation and altered cell-cycle/differentiation programs. These data indicate Omicron can engage stromal and early hematopoietic compartments and remodel stress-responsive hematopoiesis.
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