Therefore, viruses are capable of utilizing host-derived lipid membranes in their intercellular transmission to conceal and evade the host’s immune system (Izquierdo-Useros et al., 2010). Bypassing host surveillance allows augmented, unrestrained virus replication during early stages of infection (Channappanavar and Perlman, 2017). Failure of host to curb endogenous transmission at the incipient stage could contribute to aggravated disease severity and adverse outcome, such as lymphopenia leading to sudden episodes of “cytokine storm” (Zhang et al., 2020) and lethal pneumonia (Guan et al., 2020), which are the characteristic features of severe COVID-19 cases. As the primary targets of SARS-CoV-2, the alveolar type II epithelial cells synthesize surfactant phospholipids critical for modulating lung function (Schmitz and Müller, 1991), which are continuously secreted and recycled via the endocytic pathway. Exosomes, which had been isolated from broncho-alveolar lavage fluid, mediate intercellular communication between alveolar macrophages and alveolar epithelial cells that form the frontiers of host defense and immunity against air-borne pathogens (Lee et al., 2018). Therefore, it would be worthwhile to investigate if host-derived exosomes in the circulation were implicated in the pathogenesis of COVID-19.