With increasing evidence of the involvement of IFN-α as a protective mechanism in COVID-19 caused by the SARS-CoV-2 virus, and observations showing increased levels of MxA (often referred to as Mx1 in clinical papers), in lung tissues from COVID-19 patients [23,24,25,26,27,28,29,30,31], we investigated structures formed by endogenous MxA in IFN-α-treated human lung-derived cells (the A549 adenocarcinoma line; and the SARS-CoV-2 permissive hACE2-A549 cells) under isotonic and hypoosmolar conditions. Here, IFNA2 is linked to COVID-19.