A new study published in Science has uncovered possible explanations for the lingering symptoms experienced by individuals with long COVID, a condition where symptoms persist after a SARS-CoV-2 infection. The research suggests that dysregulation of the blood clotting and immune systems could be contributing factors. The study, which included 113 individuals with confirmed SARS-CoV-2 infection, found changes in the complement pathway and increased activation of the coagulation pathway in patients with long COVID symptoms at the six-month mark.
The complement system, responsible for the immune response against pathogens and damaged tissue, showed alterations in patients with long COVID compared to healthy individuals. Notably, increased activation of the complement pathway and formation of the terminal complement complex were observed in patients with long COVID, potentially leading to tissue damage. The study also revealed increased expression of molecules involved in terminal complement complex formation through the classical and alternative pathways.
Furthermore, patients with long COVID at the six-month mark exhibited lower levels of antithrombin III, an enzyme that inhibits thrombin and promotes blood coagulation. This decrease in antithrombin III levels was accompanied by increased expression of markers of thrombosis, indicating the formation of blood clots. These findings suggest a potential link between inflammation, blood clotting, and long COVID, a phenomenon referred to as thromboinflammation.
The study also identified several predictors of long COVID, including changes in complement protein levels, coagulation system biomarkers, age, and body mass index. These findings emphasize the importance of cardiovascular health assessment in individuals with long COVID at both six and twelve months.
Additionally, the study found that patients with long COVID had increased antibodies against cytomegalovirus, a type of herpesvirus. This suggests that the activation of the complement system may be triggered by the binding of antibodies to proteins from the herpesvirus. Targeting both the herpesvirus and SARS-CoV-2 with antiviral therapies could potentially alleviate long COVID symptoms.
These findings provide valuable insights into the dysregulation of the immune and coagulation systems in patients with long COVID. This understanding could contribute to the development of diagnostic tools and targeted therapies for this debilitating condition. Further research is needed to fully comprehend the underlying mechanisms of long COVID and to develop effective interventions for those affected.