УДК: 616.5-002.2-056.25-053.2:613.221]-07:616.017

Introduction. It is now known that 30% of patients who have recovered from COVID-19 develop long-COVID. According to researchers, the reactivation of herpesviruses plays a significant role in triggering long-COVID. In these patients, alteration in lymphocyte populations and T-lymphocyte subpopulations have been observed, yet the nature of these changes remains unclear. The dysregulation of the immune response caused by SARS-CoV-2 is further exacerbated by the reactivation of human herpesvirus type 6 (HHV-6). Therefore, it is essential to distinguish immune response alterations in long-COVID patients based on HHV-6 reactivation and consider these differences when developing therapeutic approaches.

The aims of this study were: 1) to investigate the associative relationships between the number of lymphocyte populations, T-lymphocyte subpopulations, and the severity of the clinical course of COVID-19 in patients with long-COVID; 2) to determine and compare the percentages of CD3+, CD4+, CD56+, CD8+, CD4/25/127– T-regs and CD19+ cells in long-COVID patients depending on the presence of reactivated HHV-6.

Materials and methods. In our study, we examined 124 patients, including 73 women (59%) and 51 men (41%), with an average age of 43±9.70 years, all of whom had suffered from COVID-19 in the second half of 2023. To confirm HHV-6 reactivation and form study groups, molecular genetic studies (PCR) were conducted on all patients. Subsequently, flow cytometry was used to analyze the lymphocyte populations and subpopulations in peripheral blood samples from the patients.

Results. In patients with long-COVID following severe COVID-19, the percentage of CD3+ T cells, CD8+ cells, and CD4+CD25+CD127– T-regs was significantly lower both in the absence of HHV-6 reactivation (p=0.014; p=0.016; p=0.045, respectively) and during the active phase of HHV-6 reactivation (p=0.045; p=0.005; p=0.008, respectively), compared to the control group. CD4+ T cells were significantly decreased only during the active phase of the herpesvirus (p=0.045). Notably, in the active phase of HHV-6, these cells were further reduced compared to those without herpesvirus reactivation. Additionally, the number of CD19+ B cells was significantly elevated in patients with HHV-6 reactivation, compared to both the control group (p<0.0001) and patients without HHV-6 reactivation (p=0.0002). Furthermore, the percentage of CD56+ NK cells in patients with long- COVID following mild and moderate COVID-19 in the history, without HHV-6 reactivation, did not differ significantly from the control group. However, NK cells were significantly lower in patients with long-COVID after severe COVID-19 in the context of HHV-6 reactivation (p=0.0001).

Conclusions. Our data confirm that HHV-6 reactivation after COVID-19 plays a role in the development of long-COVID. This is mediated through dysregulation of adaptive immune cell interactions, activation of the NF-κB signaling pathway, and increased production of antibodies with defective structure. Based on our results, patients with long- COVID following severe COVID-19, in the context of HHV-6 reactivation, may have an elevated risk of immunopathological complications, potentially including autoimmune disorders. These findings offer valuable insights for future research and potential therapeutic strategies.

In early July 2024, a prominent Ukrainian scientist, educator and historian of medicine, Professor Yaroslav Volodymyrovych Ganitkevych, celebrated his 95th birthday. A Doctor of Medicine, a full member of the Shevchenko Scientific Society (SSS) and an honorary member of the Ukrainian Medical Society (UMS), he left a memorable mark in Ukrainian medicine. His numerous works on the history of medicine, scientific heritage, and active work in medical
education have become significant assets for science and society.
Keywords: Yaroslav Ganitkevych, history of medicine, Shevchenko Scientific Society (SSS),
SSS Medical Commission 

Cutaneous syndrome is a relevant issue not only among allergic diseases but also among autoimmune disorders. Urticaria is a widespread problem, as its prevalence among the population can reach up to 9%. The main goal of the article is to analyze the role of platelet-activating factor in patients with
hypersensitive vasculitis, autoimmune, and allergic urticaria. Urticarial rash is at the intersection of allergic and autoimmune diseases, where is observed active immunopathogenetic influence of plateletactivating factor in the initiation and maintenance of systemic vasculitis, including hypersensitive/urticarial and cryoglobulinemic vasculitis Considering the significant role of this factor in the pathogenesis of hypersensitive vasculitis and allergic reactions, selective targeting of plateletactivating factor represents a promising therapeutic approach. These include plateletactivating factor receptor antagonists such as
rupatadine and apafant, as well as plateletactivating factor acetylhydrolase inhibitors, enzymes responsible for platelet-activating factor degradation. Targeted intervention on platelet-activating factor holds promise for the improving the quality of life of patients with hypersensitive vasculitis, autoimmune disorders, and allergic urticaria.
Keywords: platelet activation factor, hypersensitive vasculitis, urticaria.