A vasculo-proliferative process may contribute to long COVID, according to a new study appearing in the Journal of Translational Medicine. Researchers in Canada analyzed the plasma proteomes of patients with mild or severe acute COVID-19, patients with long COVID, and healthy individuals. They uncovered differences in the proteomes of the long COVID patients suggesting that their natural killer cells shifted their phenotype from resting to active and that their neutrophils are more likely to form extracellular traps. The researchers likewise found signaling pathway changes, including evidence that a vascular proliferative state linked to the hypoxia inducible factor 1 pathway could influence the transition from acute COVID-19 to long COVID. "When we identify these signaling patterns within the blood plasma, we can then take the information and screen drug databases to better understand which drugs would be best to target the changes we identified in long COVID patients," senior author Douglas Fraser from Ontario's London Health Sciences Centre says in a statement. "With this understanding, the identified drugs may be used in future long COVID clinical trials."