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<p>Severe COVID-19 associates with humoral immune response dysregulation. While antibodies confer protection against SARS-CoV-2, evidence also support their putative contribution to disease severity. Our study demonstrates that higher levels of S2-IgG, and S2-, RBD-, and Nucleocapsid-IgA differentiate severe and non-severe cases. However, no major antibody functional differences are found between both COVID-19 manifestations. Enhanced Fc-dependent functions in severe cases are primarily driven by increased antibody titers. No differences in antibody avidity are found between severe and non-severe cases, but a gradation in binding strength across specificities suggests that early anti-RBD, -S2, and -Nucleocapsid antibodies may originate from different pathways. In golden Syrian hamsters, S2 immunization or transfer of RBD-depleted antibodies isolated from severe and non-severe cases promote a faster clinical recovery after SARS-CoV-2 challenge, despite a transient initial weight loss. These findings indicate that antibodies are not major determinants of COVID-19 severity and suggest additional factors influencing disease outcomes.</p>

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Anti-SARS-CoV-2 antibodies from severe COVID-19 individuals or S2 immunizations do not worsen disease in hamsters

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Núria Pedreño-López,
  • Ferran Tarrés-Freixas,
  • Carla Usai,
  • Dalia Raïch-Regué,
  • Susana Benet,
  • Erola Ainsua-Enrich,
  • Julieta Carabelli,
  • Edwards Pradenas,
  • Carlos Ávila-Nieto,
  • Núria Roca,
  • Guillermo Cantero,
  • Mònica Pérez,
  • Maria Luisa Rodríguez de la Concepción,
  • Marina Matilla,
  • Boris Revollo,
  • Agnes Hernández,
  • Jorge Abad-Capa,
  • Beatriz Mothe,
  • Jose Moltó,
  • Lourdes Mateu,
  • Marta Massanella,
  • Nuria Izquierdo-Useros,
  • Julià Blanco,
  • Bonaventura Clotet,
  • Joaquim Segalés,
  • Júlia Vergara-Alert,
  • Jorge Carrillo

摘要

Severe COVID-19 associates with humoral immune response dysregulation. While antibodies confer protection against SARS-CoV-2, evidence also support their putative contribution to disease severity. Our study demonstrates that higher levels of S2-IgG, and S2-, RBD-, and Nucleocapsid-IgA differentiate severe and non-severe cases. However, no major antibody functional differences are found between both COVID-19 manifestations. Enhanced Fc-dependent functions in severe cases are primarily driven by increased antibody titers. No differences in antibody avidity are found between severe and non-severe cases, but a gradation in binding strength across specificities suggests that early anti-RBD, -S2, and -Nucleocapsid antibodies may originate from different pathways. In golden Syrian hamsters, S2 immunization or transfer of RBD-depleted antibodies isolated from severe and non-severe cases promote a faster clinical recovery after SARS-CoV-2 challenge, despite a transient initial weight loss. These findings indicate that antibodies are not major determinants of COVID-19 severity and suggest additional factors influencing disease outcomes.