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Updated: Sep 18, 2025

Isolation and Quantification of Epstein-Barr Virus from the P3HR1 Cell Line
Published on: September 28, 2022
The SARS-CoV-2 trigger highlights host interleukin 1 genetics in Epstein-Barr virus reactivation
Petra Schneiderova1, Jan Mizera2, Arootin Gharibian3
1Department of Immunology, Faculty of Medicine and Dentistry, Palacký University Olomouc and University Hospital Olomouc, Olomouc, Czech Republic.
Epstein-Barr virus (EBV) reactivation is more common in individuals with specific interleukin-1 (IL1) gene variations and SARS-CoV-2 infection. High anti-VCA IgA levels indicate recent EBV reactivation linked to long COVID pulmonary issues.
Area of Science:
- Immunology
- Virology
- Genetics
Background:
- Epstein-Barr virus (EBV) reactivation is implicated in autoimmune diseases and cancers.
- Long COVID (LC) symptoms following SARS-CoV-2 infection may involve EBV reactivation.
- Interleukin-1 (IL1) gene polymorphisms are associated with immune responses.
Purpose of the Study:
- To investigate the link between SARS-CoV-2 infection, long COVID, EBV reactivation, and host genetics.
- To identify serological markers and genetic factors associated with EBV reactivation in LC patients.
Main Methods:
- Analysis of a large cohort of SARS-CoV-2 infected individuals with LC symptoms.
- Assessment of serological markers for recent EBV reactivation (VCA IgM, VCA IgA, EA IgG).
- Evaluation of host IL1 and IL10 genetics and immune response.
Main Results:
- Recent EBV reactivation was more frequent in individuals with genetic risk in IL1RN, IL1A, and IL1B genes.
- An elevated IL-1 receptor antagonist (IL-1Ra)/IL-1β ratio and higher latent EBV load were observed.
- High anti-VCA IgA levels strongly indicated recent EBV reactivation and correlated with pulmonary dysfunction in LC.
Conclusions:
- Host IL1 genetics are associated with EBV reactivation.
- Recent EBV reactivation, marked by anti-VCA IgA, is linked to objective pulmonary dysfunction in long COVID.
- Understanding these associations may elucidate pathomechanisms of autoimmune conditions and EBV-related cancers.
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