Effect of Immunity to SARS-CoV-2 Virus on Blood Cellular Composition

Abstract

Relevance. The new coronavirus infection (COVID-19) is still a public health problem and a threat to socio-economic well-being. Most studies have focused predominantly on humoral immunity, and there are no data on the cellular composition of blood in dynamics. Aim. To study the dynamics of changes in blood cellular composition depending on the type of immunity formed (natural, hybrid, breakthrough, postvaccinal) to SARS-CoV-2 virus. Materials and Methods. A total of 130 volunteers participated in the study. Immunophenotyping of peripheral blood leukocytes using flow cytometry was performed. The presence of specific IgG antibodies to N-protein SARS-CoV-2, total IgA and cytokines (IL-4, IL-10, IFN-γ, TNF-α) was assessed in serum by ELISA. Results and Discussion. A statistically significant increase in BL was recorded in volunteers with hybrid immunity 1 month (14,0% (12,3–16,4%)) after vaccination compared to healthy volunteers (9,1% (6,4–10,2%), p = 0,0007) and people with primary COVID-19 infection (10,2% (8,3–12,1%), p = 0,0134). In volunteers with natural and hybrid immunity, as well as in revaccinated people, an increase in B1-cells (CD3-CD19+CD5+CD27-) was observed during 3–9 months of observation. It is shown that the increase of B-lymphocytes with «switched» class of synthesized antibodies was detected in people with breakthrough immunity. Increased levels of T-lymphocytes expressing HLA-DR were recorded in all individuals during 6–9 months of follow-up. Volunteers with breakthrough immunity showed a significant increase in the positivity index when assessing the presence of specific IgG class antibodies to the coronavirus N-protein compared with volunteers with natural and hybrid immunity. Conclusions. Vaccination promotes protective immunity sufficient for timely activation of memory T- and B-cells in breakthrough immunity and maintenance of immunologic efficacy in hybrid immunity against COVID-19. The results help to assess the strain of innate and adaptive immunity in novel coronavirus infection and to fill gaps in the understanding of immunopathogenesis in COVID-19.