Abstract
In confirmation of this, interestingly, a number of ILI-related viral pathogens (i.e. respiratory syncytial virus and influenza virus) have been reported to cause a significant downregulation of ACE2 in the upper and lower respiratory tract, since the early stage after the onset of infection [5]. The consequent reduction of ACE2 activity has been found potentially contributing to severe lung injury and may predispose to a later more severe clinical course of COVID-19 [6]. [...]considering that intercurrent viral respiratory infections are a trigger of upper airway mucosal damage and local immune impairment, previous ILI could therefore represent a predisposing factor for subsequent COVID-19 infection. Angiotensin-converting enzyme 2 inhibits lung injury induced by respiratory syncytial virus.
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