{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T11:04:30Z","timestamp":1790334270094,"version":"4.1.0"},"reference-count":90,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:00:00Z","timestamp":1790294400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Epstein-Barr virus (EBV) infection is ubiquitous, affecting over 90% of the global population, and while typically benign, it can rarely cause acute liver failure \u2014 a life-threatening complication that is frequently fatal. This review comprehensively reviews two overlapping clinical and pathogenetic patterns of EBV-associated hepatic failure \u2014 isolated severe EBV hepatitis and EBV-triggered hemophagocytic lymphohistiocytosis (HLH) \u2014 which are best understood as ends of a clinical spectrum rather than discrete entities. In isolated EBV hepatitis, liver injury is driven by CD8-positive T cells attacking EBV-infected B cells, causing bystander hepatocyte necrosis; inflammation remains confined to the liver, and supportive care is usually sufficient. By contrast, EBV-HLH involves EBV-infected monoclonal T or natural killer cells triggering a systemic cytokine storm (including interferon-gamma, tumor necrosis factor-alpha, interleukin-6, and interleukin-18) with hemophagocytosis, requiring immediate immunosuppression. In one pediatric cohort, an EBV DNA load exceeding 100,000 copies per milliliter was associated with a more than ten-fold increase in mortality, although no universally validated cutoff has been established across age groups or sample types; T-cell EBV DNA load provides additional prognostic information. Blood purification is an experimental adjunctive strategy in refractory cases, supported by very low-certainty evidence. We also discuss risk factors, diagnostic algorithms (including EBV DNA load, HLH-2004 criteria, and histopathology), therapeutic strategies (supportive care, antiviral therapy, immunomodulation, and liver transplantation), and future research priorities. Early recognition of HLH is life-saving. This review provides a practical clinical framework for differentiating these two entities and highlights knowledge gaps for future investigation.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1982338","type":"journal-article","created":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T10:18:57Z","timestamp":1790331537000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Epstein-Barr virus and hepatic failure: pathogenesis, clinical manifestations, and management"],"prefix":"10.3389","volume":"17","author":[{"given":"Wen","family":"Wang","sequence":"first","affiliation":[{"name":"The Second Department of Infectious Diseases, The First Affiliated Hospital of China Medical University","place":["Shenyang, Liaoning, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wen","sequence":"additional","affiliation":[{"name":"The Second Department of Infectious Diseases, The First Affiliated 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