tetano
Editor, Senior Moderator
J Microbiol Immunol Infect
. 2025 Mar 27:S1684-1182(25)00076-3.
doi: 10.1016/j.jmii.2025.03.014. Online ahead of print. COVID-19, Epstein-Barr virus reactivation and autoimmunity: Casual or causal liaisons?
Maria Cristina Tarasco[SUP] 1 [/SUP], Nicola Iacomino[SUP] 2 [/SUP], Renato Mantegazza[SUP] 2 [/SUP], Paola Cavalcante[SUP] 3 [/SUP]
Affiliations
The coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 virus infection, has been associated with a substantial risk of autoimmune disease development or exacerbation. The postulated pathophysiological mechanisms linking COVID-19 with autoimmunity include reactivation of latent Epstein-Barr virus (EBV), whose dysregulated infection in the host can trigger or promote an autoimmune response. This review summarizes recent studies highlighting a potential immunopathogenetic link between SARS-CoV-2 infection and EBV reactivation, which could underlie autoimmunity onset or worsening, as well as immune-related long COVID manifestations in COVID-19 patients. We offer our perspective on the direction that research should take to disentangle the nature (whether causal or casual) of the "COVID-19-EBV-autoimmunity" liaisons. Further advances in this research area may be crucial for designing strategies to prevent or treat EBV reactivation-related autoimmune conditions in COVID-19 patients, or patients with inflammatory co-infectious diseases, at the same time promising to improve our knowledge on the viral contribution to autoimmune phenomena.
Keywords: Autoimmunity; COVID-19; Epstein-Barr virus; Inflammation; Long COVID.
. 2025 Mar 27:S1684-1182(25)00076-3.
doi: 10.1016/j.jmii.2025.03.014. Online ahead of print. COVID-19, Epstein-Barr virus reactivation and autoimmunity: Casual or causal liaisons?
Maria Cristina Tarasco[SUP] 1 [/SUP], Nicola Iacomino[SUP] 2 [/SUP], Renato Mantegazza[SUP] 2 [/SUP], Paola Cavalcante[SUP] 3 [/SUP]
Affiliations
- PMID: 40175252
- DOI: 10.1016/j.jmii.2025.03.014
The coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2 virus infection, has been associated with a substantial risk of autoimmune disease development or exacerbation. The postulated pathophysiological mechanisms linking COVID-19 with autoimmunity include reactivation of latent Epstein-Barr virus (EBV), whose dysregulated infection in the host can trigger or promote an autoimmune response. This review summarizes recent studies highlighting a potential immunopathogenetic link between SARS-CoV-2 infection and EBV reactivation, which could underlie autoimmunity onset or worsening, as well as immune-related long COVID manifestations in COVID-19 patients. We offer our perspective on the direction that research should take to disentangle the nature (whether causal or casual) of the "COVID-19-EBV-autoimmunity" liaisons. Further advances in this research area may be crucial for designing strategies to prevent or treat EBV reactivation-related autoimmune conditions in COVID-19 patients, or patients with inflammatory co-infectious diseases, at the same time promising to improve our knowledge on the viral contribution to autoimmune phenomena.
Keywords: Autoimmunity; COVID-19; Epstein-Barr virus; Inflammation; Long COVID.