Isabelle Brock*, Anne Maitland
Coronavirus disease (COVID-19) is a heterogeneous syndrome following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection of the upper respiratory tract. ln adults, the clinical condition can range from asymptomatic cases to severe acute respiratory syndrome and multi-organ dysfunction. Those at risk of developing COVID-19 related hyper inflammatory syndrome likely had an ineffective, innate immune response to this novel pathogen. Mast cells are associated with the epithelium, contributing to tissue homeostasis and epithelial barrier defense. Equipped with an array of pathogen receptors, mast cells exhibit distinct cytokine profiles, dependent on the tissue and the triggered pathogen receptors. Following viral infections, mast cells produce pro-inflammatory chemical mediators, such as Interleukin-1 (IL-1) and IL-6, and these cytokines has been shown to be elevated in severe COVID-19 cases. Here, we present a case of a 32-year-old Caucasian woman, with Postural Orthostatic Tachycardia Syndrome (POTS), hypermobile type Ehlers Danlos Syndrome (hEDS), and a cluster of mast cell activation disorders, worrisome for a Mast Cell Activation Syndrome (MCAS), but never had laboratory confirmation of this non-clonal mast cell activation disorder, until she contracted COVID-19 in late March 2020. This case illustrates the need to recognize the rate of mast cell activation in SARS-CoV-2 infection, not only to optimize anti-SARS-CoV-2 therapy, including the development of vaccine, but to potentially curb the risk of SARS CoV-2 triggered hyper inflammatory syndrome.