Stervbo et al. (2026)
- Authors: Ulrik Stervbo, Moritz Anft, Krystallenia Paniskaki, Arturo Blazquez-Navarro, Adrian Doevelaar, Sarah Skrzypczyk, Eva Kohut, Julia Kurek, Patrizia Wehler, Sviatlana Kaliszczyk, Thorsten Brenner, Uwe Kölsch, Michael Adamzik, Michael Schmueck-Henneresse, Carmen Scheibenbogen, Sebastian Dolff, Ulf Dittmer, Oliver Witzke, Timm H. Westhoff, Nina Babel
- Institutes: Center for Translational Medicine, Medical Clinic I, Marien Hospital Herne, University Hospital of the Ruhr-University Bochum, Herne, Germany, Institute of Medical Immunology, Charité – Universitätsmedizin Berlin, Berlin, Germany, Department of Infectious Diseases, West German Centre for Infectious Diseases, University Medicine Essen, University Duisburg-Essen, Essen, Germany
- Publisher: Medical Microbiology and Immunology
- Link: DOI
Summary
This research provides a critical link between acute viral infection and the reactivation of latent herpesviruses, which is a key hypothesis in the development of Long COVID. By identifying specific T-cell markers associated with this failure of viral control, it offers a potential biological explanation for post-viral fatigue syndromes. These findings support monitoring EBV status in COVID-19 patients to better understand risks for chronic complications and post-acute sequelae.
What was researched?
The study investigated the frequency of Epstein–Barr virus (EBV) reactivation during acute COVID-19 and analyzed the specific changes in CD8 T-cell populations associated with this reactivation.
Why was it researched?
Researchers sought to understand why latent viruses like EBV often reactivate in COVID-19 patients and how this phenomenon relates to immune dysfunction and the potential development of Long COVID.
How was it researched?
The researchers analyzed biobanked blood samples from 61 patients hospitalized with moderate to critical COVID-19. They utilized flow cytometry to assess immune cell markers and quantitative PCR (qPCR) to detect viral reactivation of EBV, CMV, and HHV-6.
What has been found?
EBV reactivation was found in approximately 70% of patients across all levels of COVID-19 severity. These patients exhibited significantly lower expression of co-stimulatory markers like CD28 and CD11a on their CD8 T-cells, along with increased levels of the exhaustion marker CD57. This suggests that an altered immune state characterized by T-cell senescence is associated with the failure to control latent EBV during acute infection.
Discussion
A limitation of the study is its cross-sectional design during the first pandemic wave, which may not reflect the immune dynamics of newer viral variants. However, the high incidence of EBV reactivation regardless of COVID-19 severity is a significant finding that underscores the systemic immune impact of the virus.
Conclusion & Future Work
The study concludes that acute COVID-19 is associated with an altered CD8 T-cell phenotype indicative of replicative senescence. This impairment likely facilitates EBV reactivation, which may act as a significant driver for long-term health complications.