{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T00:34:34Z","timestamp":1790296474117,"version":"4.1.0"},"reference-count":65,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2025,10,15]],"date-time":"2025-10-15T00:00:00Z","timestamp":1760486400000},"content-version":"vor","delay-in-days":14,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Health Science Reports"],"published-print":{"date-parts":[[2025,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Severe fever with thrombocytopenia syndrome virus (SFTSV) infection causes profound dysregulation of humoral immunity, leading to immunopathology and impaired viral clearance. However, the mechanisms underlying B cell dysfunction and inadequate antibody responses remain poorly defined. This review aims to summarize current evidence on B cell\u2010mediated immune dysregulation in SFTS and explore potential therapeutic implications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We conducted a comprehensive review of recent literature on humoral immunity in SFTS, including original research articles, autopsy reports, in vitro and single\u2010cell RNA\u2010sequencing studies. We focused on B cell subset alterations, antibody production kinetics, T follicular helper (Tfh) dysfunction, germinal center disruption, and viral immune evasion mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>SFTSV preferentially targets B cells, especially plasmablasts, which become hyperactivated and serve as potential viral reservoirs. Fatal cases show excessive plasmablast expansion but fail to mount virus\u2010specific IgG responses. Disrupted germinal center formation, impaired Tfh function, and a shift toward extrafollicular antibody responses contribute to low\u2010affinity antibody production and increased autoantibody generation. Cytokine storms further suppress B and Tfh cell function. Neutralizing antibody levels correlate with survival, and delayed IgG or absent anti\u2010Gn responses are associated with poor prognosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>SFTSV requires humoral immunity by inducing pathological plasmablast proliferation, impairing Tfh\u2010B cell interactions, and suppressing protective antibody responses. Understanding these mechanisms provides insight into SFTS pathogenesis and highlights potential therapeutic targets such as germinal center restoration, plasmablast modulation, and precision immunotherapy. Future strategies should focus on vaccine design targeting conserved viral epitopes and interventions that preserve long\u2010lived B cell immunity.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/hsr2.71328","type":"journal-article","created":{"date-parts":[[2025,10,16]],"date-time":"2025-10-16T06:20:46Z","timestamp":1760595646000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Recent Advances in Humoral Immunity Dysregulation in Severe Fever With Thrombocytopenia Syndrome Virus (SFTSV) Infection: A Systematic Review"],"prefix":"10.1002","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2337-0509","authenticated-orcid":false,"given":"Hongyan","family":"Hou","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine, Tongji Hospital, Tongji Medical College Huazhong University of Science and Technology Wuhan 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