Study finds the mechanism of adenovirus vector new crown vaccine inducing thrombosis

Study finds the mechanism of adenovirus vector new crown vaccine inducing thrombosis

The study found the mechanism of the adenovirus vector new crown vaccine to induce thrombosis.

Xinhua News Agency, London, July 7 (Reporter Zhang Jiawei) A report published on the website of the British "Nature" magazine on the 7th stated that researchers at McMaster University in Canada analyzed vaccine-induced immune thrombotic thrombocytopenia (VITT) patients After the serum, it was discovered that some people experienced this rare symptom after being vaccinated with the adenovirus vector new crown vaccine, which helped to find a way to prevent this symptom and improve the safety of the vaccine
.

VITT is a rare but serious adverse reaction that occurs after vaccination with the adenovirus vector new crown vaccine, which can lead to a decrease in platelet count (thrombocytopenia) and thrombosis
.

The new crown vaccine jointly developed by AstraZeneca Pharmaceuticals in the United Kingdom and the University of Oxford and the new crown vaccine developed by Janssen Pharmaceuticals, a subsidiary of Johnson & Johnson in the United States, are all adenovirus vector vaccines

According to the report, VITT is somewhat similar to heparin-induced thrombocytopenia (HIT).
Previous studies have shown that both VITT and HIT are related to antibodies produced against platelet factor 4 (PF4)
.

But researchers have not been clear about the specific mechanism by which these antibodies cause VITT

The team analyzed the sera of five VITT patients with an average age of 44 years.
All five patients had received a dose of AstraZeneca vaccine
.

The results showed that the antibodies obtained from the sera of these patients bind to PF4 at the same sites as those of HIT patients; after comparing it with the serum samples of 10 HIT patients, the researchers found that the antibodies from VITT patients had a better binding response to PF4.

The team believes that antibodies from the serum of VITT patients bind to PF4 to form immune complexes.
These complexes then activate platelets through the FcγRIIa receptor on the platelet surface, which may cause blood clotting, leading to thrombocytopenia and thrombosis
.

But the team also pointed out that this may not be the only factor leading to thrombosis in VITT patients, and other serum factors may also be involved in platelet activation

One of the authors of the report, McMaster University researcher John Kelton said in a statement that the next step for researchers will be to develop technologies that can quickly diagnose and accurately detect VITT

This time, Nature publishes an unedited early version of the research report.

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