Bruiners Natalie, Ukey Rahul, Konvinse Katherine C, Harris Marlayna, Kalaycioglu Muge, Yang Jason H, Yang Emily, Ganapathi Usha, Honnen William, Andrews Tracy, Richlin Benjamin, Suarez Christian, Gaur Sunanda, Ricciardi Elizabeth, Hasan Uzma N, Cuddy William, Singh Aalok R, Bukulmez Hulya, Kaelber David C, Kimura Yukiko, Pinter Abraham, Napoli Stacey, Moroso-Fela Sandra, Kleinman Lawrence C, Horton Daniel B, Utz Paul J, Gennaro Maria Laura
Public Health Research Institute, Rutgers New Jersey Medical School, Newark, NJ.
Division of Allergy and Immunology, Department of Pediatrics, Stanford University, Stanford, CA.
medRxiv. 2025 Jul 23:2025.07.22.25331300. doi: 10.1101/2025.07.22.25331300.
Pediatric SARS-CoV-2 infection results in clinical presentations ranging from asymptomatic/mild infection to severe pulmonary COVID-19, to Multisystem Inflammatory Syndrome in Children (MIS-C), characterized by hyperinflammation and multi-organ involvement. While various aspects of antibody responses to pediatric SARS-CoV-2 infection manifestations have been reported, parallel studies of antibody responses to viral and self-antigens are understudied. We tested whether clinical presentations of increasing severity corresponded to different antiviral antibody and autoantibody signatures. Using custom arrays, we found that, relative to uninfected subjects, all SARS-CoV-2 infection manifestations were associated with increased autoantibody production, suggesting pediatric SARS-CoV-2 infection as a risk factor for autoimmune complications. Subtle differences were seen in autoantibody patterns among infection groups, with some autoantibodies more associated with mild manifestations and others with severe ones. When we compared MIS-C and severe COVID-19 subjects, we found differences in IgG (mostly IgG1) abundance but not in Fc-mediated effector functions. Thus, MIS-C may be associated with abnormal antibody function, suggesting that this syndrome, and perhaps other post-acute sequelae of SARS-CoV-2 infection, may be associated with antibody dysfunction. Our study shows that the antibody repertoire varies with clinical presentation of SARS-CoV-2 in children and its analysis may help understand long COVID pathogenesis.
小儿感染严重急性呼吸综合征冠状病毒2(SARS-CoV-2)会导致一系列临床表现,从无症状/轻度感染到重症新型冠状病毒肺炎(COVID-19),再到儿童多系统炎症综合征(MIS-C),其特征为过度炎症反应和多器官受累。虽然已有关于小儿SARS-CoV-2感染表现的抗体反应各个方面的报道,但对病毒抗原和自身抗原抗体反应的平行研究仍未得到充分研究。我们测试了严重程度不断增加的临床表现是否对应不同的抗病毒抗体和自身抗体特征。使用定制芯片,我们发现,与未感染的受试者相比,所有SARS-CoV-2感染表现都与自身抗体产生增加有关,这表明小儿SARS-CoV-2感染是自身免疫并发症的一个危险因素。在感染组之间的自身抗体模式中观察到细微差异,一些自身抗体与轻度表现更相关,而另一些与重度表现更相关。当我们比较MIS-C和重症COVID-19受试者时,我们发现IgG(主要是IgG1)丰度存在差异,但Fc介导的效应功能没有差异。因此,MIS-C可能与抗体功能异常有关,这表明该综合征以及也许SARS-CoV-2感染的其他急性后遗症可能与抗体功能障碍有关。我们的研究表明,抗体库随儿童SARS-CoV-2的临床表现而变化,对其进行分析可能有助于理解“长新冠”的发病机制。