Dissecting the complex pathogenesis of CAPA requires a molecular understanding of the physiological processes whereby infection with SARS-CoV-2 facilitates fungal pathogenesis. Similar to other SARS coronaviruses, SARS-CoV-2 targets and invades epithelial cells and type II pneumocytes through binding of the SARS spike protein to the angiotensin-converting enzyme 2 (ACE2) receptors [11]. Cleavage of the S1/S2 domain by the type 2 transmembrane protease TMPRSS2 leads to the activation of the spike protein [12], thereby facilitating viral entry into the target cell via ACE2. Besides its role as a SARS virus receptor, ACE2 was also demonstrated to be required for protection from severe acute lung injury in ARDS [13]. In support of this, an insertion/deletion polymorphism that affects ACE activity was associated with ARDS susceptibility and outcome [14]. Whether the preceding interaction of SARS-CoV-2 with host cells, by disrupting the regulation of the renin-angiotensin system and or the kallikrein-kinin system, contributes to the development of CAPA, is not known.