Correspondence to Author: Oussama Aazzane^1,2*, Hasnaa Bazhar ² ,Nabil Gaougaou ³ , Hassan Fellah ^1,2. 

1. Laboratory of Cellular and Molecular Pathology, Faculty of Medicine and Pharmacy, Hassan II University of Casablanca, Morocco.
2. Immunology Laboratory, Faculty of Medicine and Pharmacy, Hassan II University of Casablanca, Morocco.
3. Laboratory of Immunology and Histology, Faculty of Medicine and Pharmacy, Ibn Zohr University, Laayoune, Morocco

DOI: 10.52338/immunology.2026.5611

Abstract:

It is well known that viral infections, especially chronic ones, are associated with the development of autoimmune diseases (AID) in certain patients. In the case of COVID-19, some patients have developed disorders similar to AID. This raises the question: is COVID-19 responsible for these immune system dysfunctions, or does it merely exacerbate an underlying autoimmune pathology? It is therefore just as important to prevent the onset of these AID in certain COVID-19 positive patients as it is to fight the infection itself. To address this question, the present study aims to assess the prevalence of specific autoantibodies in COVID-19 patients, with a particular focus on IgG anti-nuclear, anti-phospholipid, anti-tissue transglutaminase, anti-deamidated gliadin, and anti-HepAk7 autoantibodies. More specifically, it seeks to identify potential immunological markers specific to SARS-CoV-2-induced autoimmunity, particularly in advanced stages of the disease (moderate to severe). This is a retrospective study conducted at the Immunology Laboratory of the Faculty of Medicine and Pharmacy in Casablanca. The analysis included 45 unvaccinated patients with confirmed SARS-CoV-2 infection and 24 healthy controls. Detection of anti-nuclear, anti-phospholipid, anti-CeliAk, and anti-HepAk7 IgG autoantibodies was performed using immunodot tests. Statistical analyses were carried out using GraphPad Prism 8 software. IgG antinuclear antibodies were detected in 6.66% of patients and 8.33% of controls, with no significant difference between groups (p = 0.799). In contrast, IgG anti-phospholipid antibodies showed significantly higher prevalence in COVID-19 patients (80%) compared to controls (0%) (p < 0.0001). IgG anti-tissue transglutaminase (anti-tTG) antibodies were found in 13.3% of patients vs. 4.2% of controls, without significant difference (p = 0.229). IgG anti-deamidated gliadin (anti-GD) antibodies were detected in 4.4% of patients and none in controls (p = 0.294). No subjects, patients or controls, were positive for IgG anti-HepAk7 antibodies (p = 1). These results highlight a significant association between SARS-CoV-2 infection and high prevalence of anti-phospholipid antibodies, supporting the hypothesis of virus-induced immune dysregulation, while the other analyzed autoantibodies (anti-nuclear, anti-tTG, anti-GD, anti-HepAk7) showed no significant differences between patients and controls. Larger prospective studies, including a broader range of autoantibodies and longitudinal follow-up, are essential to confirm these findings, assess the persistence of these abnormalities, and better understand the underlying mechanisms of COVID-19-associated autoimmunity

Keywords: Autoantibodies, Autoimmune Diseases, COVID-19.

Citation:

Dr. Oussama Aazzane, Markers Of Autoimmunity In Sars-Cov-2 Infection: Antinuclear Antibodies, Antiphospholipid Antibodies, Anti-Celiac Antibodies, And AntiHepak7 Antibodies. Journal of Immunology 2026.