The mechanism of PASC proposed in this report suggests that intermediate monocytes remain in circulation due to low CCL4 levels extending their time to differentiate leading to an accumulation of non-classical monocytes.

Further, our data suggests that interruption of the CX3CR1/fractalkine pathway could be a potential therapeutic target to reduce the survival of S1-containing non-classical monocytes and the associated vascular inflammation previously discussed.

It is important to note that the S1 protein detected in these patients appears to be retained from prior infection or phagocytosis of infected cells undergoing apoptosis and is not the result of persistent viral replication.