Immune Mutation Identified as Key Driver of Rare Vaccine-Linked Clots
An international study explains the rare VITT clotting after certain adenoviral vaccines: a viral protein mimics PF4, and a somatic mutation in an antibody gene (K31E in IGLV3-21*02/*03) redirects antibodies to PF4, activating platelets. The mutation is essential and the condition is exceedingly rare because it requires both this mutation and a common antibody-gene variant (up to 60% of people). Reversing the mutation stops the clotting in experiments, offering a blueprint for safer adenoviral vaccines and insight into other antibody-driven adverse events.
