D1.402 - Study of lymphocyte populations and subpopulations in patients with long-COVID with reactivation of herpesvirus type 6 infection
Background
Reactivation of herpesviruses occurs under conditions of immunosuppression, including that caused by SARS-CoV-2, or after intensive treatment of COVID-19. According to Vojdani A. et al. (2023), the reactivation of herpesviruses is one of the causes of long-COVID formation. In patients with long-COVID, changes in the number of populations and subpopulations of lymphocytes have been detected, but the nature of these changes has not been established.
Objective. To compare changes in the cellular component of the immune response in patients with long-COVID depending on HHV-6 reactivation.
Method
124 patients with long-COVID symptoms were examined: 59% women and 41% men, mean age 43±9.70 years, who suffered COVID-19 in the second part of 2023. Study groups were formed depending on the severity of COVID-19 in the medical history. HHV-6 reactivation was determined using molecular genetic studies (PCR). Flow cytometry was used to study patients' lymphocyte populations and subpopulations in peripheral blood samples.
Results
It was determined that the most pronounced decrease in the number of populations and subpopulations of T lymphocytes (CD3+, CD4+ & CD8+ T-cells, CD4+CD25+CD127− T-regs) was in patients with long-COVID after severe COVID-19 regardless of HHV-6 reactivation. However, only with HHV-6 reactivation was a decrease in CD4+ T cells (p=0.005) and a significant reduction in NK (p=0.0001) compared to the control group.
At the same time, the number of CD19+ B cells was higher than the control group (p<0.0001). In patients with long-COVID after mild, moderate, and severe COVID-19 in the anamnesis, a significant increase in CD19+ B cells was determined regardless of HHV-6 reactivation.
Conclusion
The data confirm that HHV-6 reactivation after COVID-19 can affect long-COVID formation. This can occur in the following ways: dysregulation of the interaction between adaptive immune cells, activation of the NF-κB signaling pathway, and increased production of antibodies with a defective structure. According to our results, patients with long-COVID after severe COVID-19 in medical history with HHV-6 reactivation will have a higher risk of immunopathological complications, including autoimmune formation.
