Clonal hematopoiesis is not significantly associated with COVID-19 disease severity
Yifan Zhou, Ruba Shalhoub, Stephanie N. Rogers, Shiqin Yu, Muxin Gu, Margarete A. Fabre, Pedro M. Quirós, Tae–Hoon Shin, Arch Diangson, Wenhan Deng, Shubha Anand, Wenhua Lu, Matthew Cullen, Anna L. Godfrey, Jacobus Preller, Jérôme Hadjadj, Emmanuelle Jouanguy, Aurélie Cobat, Laurent Abel, Frédéric Rieux‐Laucat, Benjamin Terrier, Alain Fischer, L. Novik, Ingelise J. Gordon, Larisa Strom, Martin R. Gaudinski, Andrea Lisco, Irini Sereti, Thomas J. Gniadek, Andrea Biondi, Paolo Bonfanti, Luisa Imberti, Clifton L. Dalgard, Yu Zhang, Kerry Dobbs, Helen C. Su, Luigi D. Notarangelo, Colin O. Wu, Peter Openshaw, Malcolm G. Semple, Ziad Mallat, J. Kenneth Baillie, Cynthia E. Dunbar, George S. Vassiliou
Abstract
Clonal hematopoiesis (CH) describes the disproportionate expansion of a hematopoietic stem<br/>cell (HSC) and its progeny, in association with leukemia-associated somatic mutations, most<br/>commonly affecting the genes for epigenetic regulators DNMT3A, TET2 and ASXL1.<br/>The prevalence and size of such clones rise with age, in association with changes in the driver gene landscape.10 CH is associated with an increased risk of hematologic malignancies, but also of cardiovascular disease (CVD), independently of other known CVD risk factors.11,12 The basis for<br/>this increased CVD risk has been linked to hyperinflammatory positive feedback loops driven by increased cytokine release from clonal myeloid cells, particularly interleukin IL-6 and IL-1β.