Overview
- In a paper published Feb. 11–12, 2026, an international team from McMaster, Flinders and Universitätsmedizin Greifswald reports that adenoviral protein VII (pVII) can mimic human platelet factor 4 (PF4).
- The researchers show that VITT arises only when people with IGLV3‑21*02 or *03 generate a rare K31E somatic mutation that redirects antibodies from pVII to PF4 after adenoviral exposure by vaccine or natural infection.
- The K31E mutation was found in all VITT patient antibodies examined, and reversing it in engineered antibodies eliminated clot‑activating activity, findings corroborated in a humanized mouse model.
- Authors say the identified viral component can be redesigned or removed to avoid the misdirected immune response in future adenoviral vaccines, though no changes have yet been implemented.
- The mechanism helps explain observed patterns, including higher incidence after first doses and population differences, as well as the small number of severe cases documented in rollouts such as the US (60 cases, 9 deaths after ~19 million J&J doses), the UK (455 cases, 81 deaths after ~50 million AstraZeneca doses) and eight deaths in Australia.