What autoantibodies are associated with severe Coronavirus disease (COVID-19) infection?

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Last updated: February 14, 2025View editorial policy

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From the Guidelines

Autoantibodies associated with severe COVID-19 infection are not explicitly stated in the provided evidence.

Autoantibodies and COVID-19

  • The evidence suggests that high levels of autoantibodies in long COVID have been found to be inversely correlated with protective COVID-19 antibodies 1.
  • However, the specific autoantibodies associated with severe COVID-19 infection are not mentioned in the provided studies.

Immune Dysregulation

  • Studies have found T cell alterations, including exhausted T cells, reduced CD4 and CD8 effector memory cell numbers, and elevated PD1 expression on central memory cells, persisting for at least 13 months in individuals with long COVID 1.
  • Immune dysregulation with or without reactivation of underlying pathogens, including herpesviruses, has been suggested as a potential cause of long COVID 1.

Risk Factors

  • Risk factors for long COVID potentially include the presence of specific autoantibodies, although the exact autoantibodies are not specified 1.
  • Other risk factors include female sex, type 2 diabetes, EBV reactivation, connective tissue disorders, attention deficit hyperactivity disorder, chronic urticaria, and allergic rhinitis 1.

From the Research

Autoantibodies Associated with Severe COVID-19 Infection

  • Autoantibodies against type I interferons (IFNs) have been found to be associated with severe COVID-19 infection, with a positive rate of 10% (95% CI, 7-14%) in patients with severe infection 2.
  • The most common subtypes of autoantibodies against type I IFNs are anti-IFN-α (89%) and anti-IFN-ω (77%) 2.
  • Autoantibodies against immunomodulatory proteins, including cytokines, chemokines, complement components, and cell surface proteins, have been found to be prevalent in COVID-19 patients and are associated with disease severity 3, 4.
  • Autoantibody signatures, characterized by elevated concentrations of IgG and IgA autoantibodies, have been found to be associated with COVID-19 severity, with higher levels of autoantibodies found in patients with moderate or severe disease 5.
  • Autoantibodies against tissue-associated antigens have been found to be associated with specific clinical characteristics and disease severity 3, 5, 4.
  • New-onset IgG autoantibodies have been found to develop in a significant proportion of hospitalized COVID-19 patients, with autoantibodies targeting autoantigens associated with rare disorders such as myositis, systemic sclerosis, and CTD overlap syndromes 6.

Specific Autoantibodies Associated with Severe COVID-19 Infection

  • Anti-IFN-α and anti-IFN-ω autoantibodies have been found to be associated with severe COVID-19 infection 2.
  • Autoantibodies against cytokines, chemokines, complement components, and cell surface proteins have been found to be prevalent in COVID-19 patients and are associated with disease severity 3, 4.
  • Anti-nuclear antibodies (ANA) have been found to be present in approximately 25% of COVID-19 patients 6.
  • Autoantibodies against angiotensin converting enzyme-2 (ACE-2) have been found in rare patients with COVID-19 6.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Autoantibodies against type I interferons in COVID-19 infection: A systematic review and meta-analysis.

International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases, 2023

Research

Diverse Functional Autoantibodies in Patients with COVID-19.

medRxiv : the preprint server for health sciences, 2021

Research

New-Onset IgG Autoantibodies in Hospitalized Patients with COVID-19.

medRxiv : the preprint server for health sciences, 2021

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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