Clonal hematopoiesis in patients with Covid‐19 is stable and not linked to an aggravated clinical course
Abstract
To the Editor: The strength of host immune reaction to infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) determines the severity of corona virus disease 2019 (Covid-19). While a basic antiviral immune response involving innate immune mechanisms and an induction of adaptive immunity is needed to resolve the disease, particularly innate myeloid cells can also induce a dysregulated, excessive, aberrant and non-effective host immune response in severe Covid-19. The latter is termed “hyperinflammation,” “cytokine storm,” “macrophage activation syndrome” or “cytokine release syndrome.” Hyperinflammation contributes to the pathogenesis of Covid-19 related acute respiratory distress syndrome (ARDS), which is associated with a fatal outcome in the majority of patients, but may also induce multi-organ damage, which is the second most common cause of death in Covid-19. Thus, a better understanding of underlying host-intrinsic factors driving immune dysfunction is warranted for the immediate identification of patients at risk and eventually also for selecting novel targeted therapies. Thus, SARS-CoV-2 has been found to infect multiple cells expression ACE-2 receptors including human monocytes, macrophages and dendritic cells, emphasizing their contribution to disease pathology. Of relevance, clonal hematopoiesis (CH; defined as somatic variants in the peripheral blood at a variant allele frequency ≥2%) is considered to imprint inflammation in myeloid cells,…
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