The first case of COVID-19 was diagnosed in St. Petersburg on March 2, 2020; the period of increase in the incidence lasted for 10 weeks, the maximum rates were recorded in mid-May, and subsequently there was a statistically significant decrease in the incidence.Objective: to determine the level and structure of community immunity to SARS-CoV-2 among the population of St. Petersburg during the period of intensive spread of COVID-19.Materials and methods. Selection of volunteers for the study was carried out through interviewing and randomization. The exclusion criterion was active COVID-19 infection at the time of the survey. 2713 people aged 1 to 70 years and above were examined for the presence of specific antibodies to SARS-CoV-2. Antibodies were detected by enzyme immunoassay.Results and discussion. Studies have shown that in St. Petersburg, in the active phase of COVID-19 epidemic, there was a moderate seroprevalence to SARS-CoV-2, which amounted to 26 %, against the background of a high frequency (84.5 %) of asymptomatic infection in seropositive individuals who did not have a history of COVID-19 disease, positive PCR result and ARI symptoms on the day of examination. The maximum indicators of herd immunity were established in children 1–6 years old (31.1 %), 7–13 years old (37.7 %) and people over 70 years old (30.4 %). Differences in the level of seroprevalence in the age groups of 18–49 years are statistically significant. The highest level of seroprevalence was found among the unemployed (29.7 %), healthcare workers (27.1 %), education sector (26.4 %) and business sector personnel (25 %). In convalescents, COVID-19 antibodies are produced in 75 % of cases. In individuals with positive result of PCR analysis carried out earlier, antibodies are detected in 70 % of the cases. The results of the study of herd immunity to SARS-CoV-2 are essential to forecast the development of the epidemiological situation, as well as to plan measures for specific and non-specific prevention of COVID-19.

IgG is the most prominent marker of post-COVID-19 immunity. Not only does this subtype mark the late stages of infection, but it also stays in the body for a timespan of at least 6 months. However, different IgG subclasses have different properties, and their roles in specific anti-COVID-19 responses have yet to be determined. We assessed the concentrations of IgG1, IgG2, IgG3, and IgG4 against different SARS-CoV-2 antigens (N protein, S protein RBD) using a specifically designed method and samples from 348 COVID-19 patients. We noted a statistically significant association between severity of COVID-19 infection and IgG concentrations (both total and subclasses). When assessing anti-N protein and anti-RBD IgG subclasses, we noted the importance of IgG3 as a subclass. Since it is often associated with early antiviral response, we presumed that the IgG3 subclass is the first high-affinity IgG antibody to be produced during COVID-19 infection.

Background. Humoral immunity requires interaction between B cell and T follicular helper cells (Tfh) to produce effective immune response, but the data regarding a role of B cells and Tfh in SARS-CoV-2 defense are still sparse. Methods. Blood samples from patients with acute COVID-19 (n = 64), convalescents patients who had specific IgG to SARS-CoV-2 N-protein (n = 55), and healthy donors with no detectable antibodies to any SARS-CoV-2 proteins (HC, n = 44) were analyses by multicolor flow cytometry. Results. Patients with acute COVID-19 showed decreased levels of memory B cells subsets and increased proportion plasma cell precursors compared to HC and COVID-19 convalescent patients, whereas for the latter the elevated numbers of virgin naïve, Bm2′ and “Bm3+Bm4” was found if compared with HC. During acute COVID-19 CXCR3+CCR6− Tfh1-like cells were decreased and the levels of CXCR3−CCR6+ Tfh17-like were increased then in HC and convalescent patients. Finally, COVID-19 convalescent patients had increased levels of Tfh2-, Tfh17- and DP Tfh-like cells while comparing their amount with HC. Conclusions. Our data indicate that COVID-19 can impact the humoral immunity in the long-term.

The aggressive infectious nature of SARS-CoV-2, its rapid spread, and the emergence of mutations necessitate investigation of factors contributing to differences in SARS-CoV-2 susceptibility and severity. The role of genetic variations in the human HLA continues to be studied in various populations in terms of both its effect on morbidity and clinical manifestation of illness. The study included 484 COVID-19 convalescents (northwest Russia residents of St. Petersburg). Cases in which the responsible strain was determined were divided in two subgroups: group 1 (n = 231) had illness caused by genovariants unrelated to variant of concern (VOC) strains; and group 2 (n = 80) had illness caused by the delta (B.1.617.2) VOC; and a control group (n = 1456). DNA typing (HLA-A, B, DRB1) was performed at the basic resolution level. HLA-A*02 was associated with protection against infection caused by non-VOC SARS-CoV-2 genetic variants only but not against infection caused by delta strains. HLA-A*03 was associated with protection against infection caused by delta strains; and allele groups associated with infection by delta strains were HLA-A*30, B*49, and B*57. Thus, in northwest Russia, HLA-A*02 was associated with protection against infection caused by non-VOC SARS-CoV-2 genetic variants but not against delta viral strains. HLA-A*03 was associated with a reduced risk of infection by delta SARS-CoV-2 strains. HLA-A*30, HLA-B*49, and HLA-B*57 allele groups were predisposing factors for infection by delta (B.1.617.2) strains.

Acute disorders of cerebral circulation are one of the leading problems of modern clinical medicine, due to their significant spread in the human population and the extremely negative impact exerted on the patient’s body. Currently available data allow us to talk about the multi-vector nature of the pathogenesis of ischemic brain damage. Within the framework of the cascade of developing pathochemical and pathophysiological processes, an essential role in the formation of ischemic stroke belongs to the inflammatory reaction occurring through the immune system’s response to cerebral tissue ischemia. One of the places of its implementation is the vessel wall located in the ischemic zone, where monocytes and neutrophils are attracted with the help of cell adhesion proteins. Complement activation plays a significant role, carried out mainly due to the C3 component or during the initialization of the mannose pathway. Activation of microglia and astrocytes plays a huge role directly in the focus of ischemia. It should be noted that in the process of activation, both microglia and astrocytes are able to acquire a pro-inflammatory or anti-inflammatory phenotype. The prevalence of the pro-inflammatory variant contributes to prolonged damage to brain tissue, while the predominance of the anti-inflammatory phenotype has a protective effect. An important role is played by a violation of the function of the blood-brain barrier, which provides an additional influx of leukocytes to the site of ischemia. In addition, individual subpopulations of T-lymphocytes penetrating through the damaged barrier also play a significant role in the organization and dynamics of the immuno-inflammatory response. The action of Th1 and Th2 cells, gamma-delta T lymphocytes, natural killer cells, as well as regulatory T lymphocytes has been most studied. The role of B-lymphocytes in the formation of a stroke focus is considered.