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. 2023 Jul 4;28(12):4968–4976. doi: 10.1038/s41380-023-02161-5

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — EBV directly infects resting B cells or epithelial cells, and is then stored in the infected memory B cells of the peripheral blood that express latent membrane protein 2 (LMP-2) and EBV nuclear antigens (EBNAs). After SARS-CoV-2 infection, these B cells can cause EBV reactivation, resulting in severe systemic inflammation. As the interaction of the XBP-1 (X-box binding protein 1) with S1R (sigma-1 receptor) may play a role in EBV reactivation, sigma-1 receptor agonists (e.g., fluvoxamine) may attenuate EBV reactivation, resulting in reduced long COVID symptoms. Part of the figure was designed using resources from Biorender.com and www.irasutoya.com.