Research ArticleCORONAVIRUS

Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19

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Science Translational Medicine  18 Nov 2020:
Vol. 12, Issue 570, eabd3876
DOI: 10.1126/scitranslmed.abd3876

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  • Response to e-Letter by Battinelli et al.
    • Yu Zuo, Assitant Professor, Division of Rheumatology, University of Michigan
    • Other Contributors:
      • Jason S. Knight, Associate Professor, Division of Rheumatology, University of Michigan
      • Yogendra Kanthi, Lasker Investigator, Laboratory of Vascular Thrombosis and Inflammation, National Heart, Lung and Blood Institute

    We read with interest the letter by Battinelli and colleagues and appreciate their cogent summary of our work. We also value their new description of 24 COVID-19 patients who were negative for anticardiolipin (aCL) and anti-beta-2 glycoprotein I (aβ2GPI) antibodies.

    We very much support the premise that it is best not to rigidly apply the modified Sapporo criteria for classification of APS to patients hospitalized with moderate-to-severe COVID-19. Given the uncharted waters represented by COVID-19, it is likely that criteria to standardize the approach to autoimmunity in COVID-19 will need to be devised anew. Furthermore, while “criteria antiphospholipid antibodies” including aCL IgG/IgM, aβ2GPI IgG/IgM, and lupus anticoagulant are the most tested and easily assessable in all clinical settings, there are also a number of non-criteria antiphospholipid antibodies such as anti-phosphatidylserine/prothrombin (aPS/PT) and anti-domain I β2GPI that are biologically relevant and show promising clinical utility in identifying individuals with antiphospholipid syndrome (1-5). We therefore agree that the mechanistic role of non-criteria antiphospholipid antibodies in driving thromboinflammation warrants further evaluation.

    Our studies prior to the current pandemic have demonstrated the thrombotic potential of purified antiphospholipid antibodies (6, 7), which lends additional context to the current research. Here, we observed that purified IgG fractions isolated from p...

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    Competing Interests: None declared.
  • RE: Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19
    • Elisabeth M. Battinelli, Corresponding Author/Hematologist, Brigham and Women's Hospital
    • Other Contributors:
      • Nathan T. Connell, Author/Hematologist, Brigham and Women's Hospital
      • Lachelle D. Weeks, Author/Hematologist, Brigham and Women's Hospital
      • Jean M. Connors, Author/Hematologist, Brigham and Women's Hospital

    Response to:
    Zuo Y, Estes SK, Ali RA, et al. Prothrombotic autoantibodies in serum from patients hospitalized with COVID-19. Sci Transl Med. 2020.

    Elisabeth M. Battinelli, Nathan T. Connell, Lachelle D. Weeks and Jean M. Connors
    Brigham and Women’s Hospital, Division of Hematology, Boston, MA

    Corresponding Author: Elisabeth M. Battinelli

    One of the hallmarks of COVID-19 infection is abnormal coagulation characteristics and an increased thrombotic risk.1,2 The etiology of this aberrant thrombosis is thought to be due to cytokine storm leading to damaged endothelium and activation of leukocytes and platelets as well as direct activation of immune cells and the endothelium by the virus itself.3 Zuo and colleagues describe the presence of antiphospholipid (aPL) antibodies at one time point and suggest that these autoantibodies may contribute to the elevated risk of thrombosis in COVID-19.4 This is not the first time that aPLs have been noted in COVID-19 patients.5 The authors have compiled a panel of eight antiphospholipid antibodies and assessed the serum of 172 patients hospitalized with COVID-19. They found that 24% of the patient samples had elevated anti-phosphatidylserine/prothrombin (aPS/PT) IgG, 23% had elevated anticardiolipin (aCL) IgM, and 18% elevation in aPS/PT IgM. The authors demonstrated in in vitro studies that higher titers of aPL antibodies we...

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    Competing Interests: None declared.

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