Figure 1. Following SARS-CoV-2 infection, blood-borne competent mitochondria provide a novel source of restorative ATP and constitutive nitric oxide synthase (cNOS) to stimulate the release of nitric oxide (NO), which is anti-inflammatory.

During acute stress from viral infection, proinflammatory responses partially mediate autoregulatory homeostatic mechanisms and maintain immune surveillance against infection [18]. Changes in the production of proinflammatory mediators commonly occur in autoimmune diseases and comorbid syndromes [18]. Cell-free mitochondria with significant bioenergetics capacity are present in the peripheral circulation [1]. Blood-borne competent mitochondria may represent a novel source of restorative ATP. Also, cNOS activation results in enhanced production, release, and intra-mitochondrial recycling of NO, which promote anti-inflammatory processes, to effectively modulate cell damage following viral infection [19].