COVID-19 deteriorates type II pneumocytes and damages the alveolar immunologic balancing process through the inadvertent activation of a sequence of localized and general inflammatory responses. Due to an aggregation of uncleaved angiotensin II, the stimulated inflammatory cells cause cytokines synthesis and secretion (cytokine storming). The cytokines cause the systemic inflammatory response syndrome (SIRS), leading to widespread tissue injuries. Consequently, pro-coagulant factors are activated which increases the microthrombi in different tissues, resulting in ischemia, multiple organ dysfunction syndrome, acute respiratory distress syndrome, and increased mortality. Vaccines recipients (via virus vector technology) have reported the incidence of thrombocytopenia and peculiar thrombotic events. After vaccination, using sera from patients who experienced thrombocytopenia and thrombosis showed increased reactivity in anti-PF4/heparin enzyme immunoassays and substantial platelet-activating antibodies (positive). In some sera of individuals suffering from heparin-induced thrombocytopenia (HIT), it has been observed that platelet-activating antibodies resulting from vaccination tend to bind to non-complexed PF4 alone.
Thrombosis Formation after COVID-19 Vaccination Immunological Aspects: Review Article