| First Author | Rommel MGE | Year | 2022 |
| Journal | Cell Rep | Volume | 41 |
| Issue | 1 | Pages | 111447 |
| PubMed ID | 36198277 | Mgi Jnum | J:329915 |
| Mgi Id | MGI:7355913 | Doi | 10.1016/j.celrep.2022.111447 |
| Citation | Rommel MGE, et al. (2022) Influenza A virus infection instructs hematopoiesis to megakaryocyte-lineage output. Cell Rep 41(1):111447 |
| abstractText | Respiratory tract infections are among the deadliest communicable diseases worldwide. Severe cases of viral lung infections are often associated with a cytokine storm and alternating platelet numbers. We report that hematopoietic stem and progenitor cells (HSPCs) sense a non-systemic influenza A virus (IAV) infection via inflammatory cytokines. Irrespective of antiviral treatment or vaccination, at a certain threshold of IAV titer in the lung, CD41-positive hematopoietic stem cells (HSCs) enter the cell cycle while endothelial protein C receptor-positive CD41-negative HSCs remain quiescent. Active CD41-positive HSCs represent the source of megakaryocytes, while their multi-lineage reconstitution potential is reduced. This emergency megakaryopoiesis is thrombopoietin independent and attenuated in IAV-infected interleukin-1 receptor-deficient mice. Newly produced platelets during IAV infection are immature and hyper-reactive. After viral clearance, HSC quiescence is re-established. Our study reveals that non-systemic viral respiratory infection has an acute impact on HSCs via inflammatory cytokines to counteract IAV-induced thrombocytopenia. |
