Epstein-Barr virus-acquired immunodeficiency in myalgic encephalomyelitis-Is it present in long COVID?
Keywords: 
Área de Medicina Clínica y Epidemiología
Chronic fatigue syndrome
Infammation
HLA-II alleles
Immunodefciency
Post-acute COVID-19 syndrome
EBV EBNA-1
Long COVID syndrome
Myalgic encephalomyelitis
Issue Date: 
2023
ISSN: 
1479-5876
Note: 
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Citation: 
Ruiz-Pablos, M.; Lourenco-Paiva, B. (Bruno David); Zabaleta-Azpiroz, A. (Aintzane). "Epstein-Barr virus-acquired immunodeficiency in myalgic encephalomyelitis-Is it present in long COVID?". Journal of translational medicine. 21 (1), 2023, 633
Abstract
Both myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS) and long COVID (LC) are characterized by similar immunological alterations, persistence of chronic viral infection, autoimmunity, chronic inflammatory state, viral reactivation, hypocortisolism, and microclot formation. They also present with similar symptoms such as asthenia, exercise intolerance, sleep disorders, cognitive dysfunction, and neurological and gastrointestinal complaints. In addition, both pathologies present Epstein-Barr virus (EBV) reactivation, indicating the possibility of this virus being the link between both pathologies. Therefore, we propose that latency and recurrent EBV reactivation could generate an acquired immunodeficiency syndrome in three steps: first, an acquired EBV immunodeficiency develops in individuals with weak EBV HLA-II haplotypes, which prevents the control of latency I cells. Second, ectopic lymphoid structures with EBV latency form in different tissues (including the CNS), promoting inflammatory responses and further impairment of cell-mediated immunity. Finally, immune exhaustion occurs due to chronic exposure to viral antigens, with consolidation of the disease. In the case of LC, prior to the first step, there is the possibility of previous SARS-CoV-2 infection in individuals with weak HLA-II haplotypes against this virus and/or EBV.

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