Epstein-Shuman Adam, Hunt Joanne H, Caturegli Patrizio, Winguth Patrick, Fernandez Reinaldo E, Rozek Gracie M, Zhu Xianming, DiRico Nicholas A, Jamal Armaan, Hsieh Yu-Hsiang, Manabe Yukari C, Redd Andrew D, Reynolds Steven J, Antar Annukka A R, Laeyendecker Oliver
Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Int J Infect Dis. 2025 Jan;150:107289. doi: 10.1016/j.ijid.2024.107289. Epub 2024 Nov 1.
Autoantibodies (AAbs) directed against interferon alpha (aIFNα), nuclear antigens (ANAs), anti-cardiolipin (aCL), and anti-beta 2 glycoprotein 1 (aβ2GP1), have been demonstrated to significantly correlate with the severity of acute Coronavirus Disease 2019 (COVID-19). However, whether severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection induces these AAbs and whether they are associated with long COVID remains unclear.
The potential induction of aIFNα, ANAs, aCL, and aβ2GP1 by SARS-CoV-2 was assessed by measuring these AAbs in 224 pre- and post-infection paired serum samples from the Johns Hopkins Hospital Emergency Department (JHHED). The relationship between these AAbs and long COVID was assessed using 60 serum samples from participants in the Outpatient SARS-CoV-2 Mild and Asymptomatic Infection Response and Transmission study.
We found no evidence that these AAbs were induced in the JHHED cohort and no significant difference in their prevalence between patients with (n = 30) and without (n = 30) long COVID in the OutSMART cohort.
These findings do not support the hypotheses that SARS-CoV-2 induces these AAbs or that they are related to long COVID.
已证实，针对α干扰素（aIFNα）、核抗原（ANA）、抗心磷脂（aCL）和抗β2糖蛋白1（aβ2GP1）的自身抗体（AAb）与2019年新型冠状病毒病（COVID-19）的严重程度显著相关。然而，严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染是否会诱导产生这些AAb，以及它们是否与长期COVID相关仍不清楚。
通过检测约翰霍普金斯医院急诊科（JHHED）224例感染前后配对血清样本中的这些AAb，评估SARS-CoV-2对aIFNα、ANA、aCL和aβ2GP1的潜在诱导作用。使用门诊SARS-CoV-2轻症和无症状感染反应及传播研究参与者的60份血清样本，评估这些AAb与长期COVID之间的关系。
我们没有发现证据表明在JHHED队列中这些AAb被诱导产生，并且在OutSMART队列中，患有（n = 30）和未患有（n = 30）长期COVID的患者之间，它们的流行率没有显著差异。
这些发现不支持SARS-CoV-2诱导产生这些AAb或它们与长期COVID相关的假设。
