期刊
VACCINE
卷 40, 期 13, 页码 1996-2002出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.vaccine.2022.02.037
关键词
Animals; Blood coagulation; Blood platelets; COVID-19; Thrombosis; Vaccines
资金
- National Science Centre in Poland [2016/23/N/NZ7/00442]
- Medical University of Bialystok [SUB/2/DN/20/001/2211]
In this study, it was found that ChAdOx1 nCoV-19 vaccine does not increase the risk of arterial thrombosis development in female rats. Vaccinated rats developed SARS-CoV-2-specific neutralizing antibodies, and there were slight luminal narrowing and extravasation of blood in the blood vessel/thrombus area. However, there were no significant differences in thrombus weight and composition, and only a slight increase in platelet aggregation was observed.
ChAdOx1 nCoV-19 adenoviral vector vaccine (ChAd) against coronavirus disease 2019 has been associated with vaccine-induced thrombosis and thrombocytopenia (VITT), especially in young women who have presented with unusual localized thrombosis after receiving the vaccine. The pathogenesis of VITT remains incompletely understood. We tried to provide new insights into mechanisms underlying this phenomenon in the model of arterial thrombosis electrically induced in the carotid artery of female rats. At 28 days post-vaccination, ChAd induced SARS-CoV-2-specific neutralizing antibody responses in all animals. The analysis of the blood vessel/thrombus area showed slight luminal narrowing of the carotid artery with extravasation of blood in vaccinated rats. These small changes were not accompanied by differences in thrombus weight and composition. The vaccinated animals presented a slight increase (by around 14-24%) in platelet aggregation. ChAd did not significantly affect blood coagulation, platelet counts, and their activation markers. Unaffected thrombus formation, the lack of thrombocytopenia and all the measured blood and hemostasis parameters that predominantly stayed unchanged, indicate that the ChAd does not increase the risk of arterial thrombosis development in female rats. (c) 2022 Elsevier Ltd. All rights reserved.
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