Abstract Topic: 30. Infections in hematology (incl. supportive care/therapy)
Background: One of the features of COVID-19 infection is an immune-mediated hypercoagulable state with impaired microcirculation, arterial and venous thrombosis, and the development of multi-organ failure. In this regard, patients with thrombophilia (TF), initially predisposed to the development of thrombotic events, require special attention in relation to severe complications of COVID-19. The probability of any specific immune disorders in this group of patients is not excluded. It is known that clinical and laboratory abnormalities, including parameters of cellular and humoral immunity, can persist for a long time after a COVID-19 infection.
Aims: to study distinctive features of immune system disturbances in the post-COVID period in patients with hereditary thrombophilia.
Methods: The following groups were examined: patients with hereditary TF within 6 months after COVID-19 infection (group A, n=26); persons with TF who did not undergo COVID-19 (group B, n=21); persons without hemostasis pathology who were examined within 6 months after COVID-19 (group C, n=119), and healthy donors (control group D, n=43). We evaluated the subsets of lymphocytes expressing CD3, CD4, CD8, CD16, CD25, HLA-DR and T-regulatory cells (Treg), the levels of total serum immunoglobulins of classes G, A and M, circulating immune complexes with low (CIClow) or medium (CICmed) molecular weight, and the level of specific anti-SARS-CoV-2 IgG antibodies by ELISA.
Results: When assessing changes in immune parameters in persons without TF who underwent COVID-19 (comparison of groups C and D) within 6 months, a moderate increase in the percent amount of T-helpers (CD3+CD4+), T-regulatory (CD25+CD4+) and activated T-cells (CD3+HLA-DR+) was observed, as well as the CIC, in particular, CEClow, while the level of B-cells (CD19+) and IgA decreased slightly. When assessing the immune parameters in persons with TF who had not undergone COVID-19 (group B), the following differences were noted compared with the donor group (D): an increased percent of T-helpers (48.5% vs. 42.6% respectively, p < 0.01), reduced CD3+CD16+ lymphocytes (1.0% vs. 4.6% respectively, p < 0.001), significant increase in the level of CECmed (55.7 units vs. 34.1 units respectively) and CEClow (344 units vs. 122.5 units respectively).
The tendency of immune disturbances after COVID-19 infection in patients with TF (comparison of groups A and B) was basically similar to those in persons without hemostasis pathology. However, the characteristic features of the group with TF in the post-COVID period were the tendency to decrease in T-helpers and CD4+/CD8+ ratio, the absence of significant changes in the content of T-regulatory cells. Significant differences between groups A and C were observed in the level of specific anti-SARS-CoV-2 IgG antibodies: 726.9 BAU/mL and 207.5 BAU/mL (p < 0.05). Besides, for TF patients a direct correlation (p < 0.05) of the level of antibodies with the content of cytotoxic (CD3+CD8+) and activated (CD3+HLA-DR+) T cells was observed.
Summary/Conclusion: Thus, in the post-COVID period in patients with TF, the main immunological changes are similar to those in patients without hemostasis pathology. However, this group have demonstrated a tendency to a decrease in T-helpers and CD4+/CD8+ ratio, and the absence of significant changes in the content of T-regulatory cells with an increased level of antibody production.
Keywords: Immune response, Thrombophilia, COVID-19