Antibodies from long COVID patients provide clues for finding triggers of autoimmunity
Long-haul COVID, or long COVID, is increasingly recognized in a significant percentage of individuals within a few months after infection with SARS-CoV-2. This condition is characterized by a wide range of persistent, recurring, or even new but related symptoms that involve various tissues and organs, including respiratory, cardiac, vascular, gastrointestinal, musculo-skeletal, endocrine, systemic, neurological and more. Thus, a multi-factorial disorder such as this cannot be diagnosed with a single blood test and treated with one single remedy.
Some overlapping symptomatologies exist between long COVID and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Very much like with long ME/CFS, infections with herpes family viruses, immune dysregulation, and the persistence of inflammation have been reported as the most common pattern for the development of long COVID. Viral superantigen activation of the immune system, disturbance in the gut microbiome, and multiple tissue damage and autoimmunity are only some of the mechanisms that have been associated with long COVID.

Among these mechanisms, persistent SARS-CoV-2 infection and superantigens released by the virus which are known to induce polyclonal activation of T cells, dendritic cells, and cytokine storm could induce apoptosis and release of cellular components, which could lead to the autoimmunity associated with long COVID. In particular, the three viruses associated with long COVID, SARS-CoV-2, Epstein-Barr Virus (EBV), and Human Herpesvirus 6/7 (HHV-6/7) have been found to be involved with the pathogenesis and progression of autoimmunity.
Autoimmune diseases affect about 10% of the world population. Their induction is due to a combination of genetic predisposition and environmental factors that affect the functioning of the immune system through various mechanisms. Among these environmental factors are infectious agents, which may not only assault and weaken the body and the immune system, but which could also induce autoimmunity through the molecular mimicry between viruses and many human tissues.
The role of autoimmunity in long COVID is supported by hundreds of published articles, some of which were based on studies conducted in our laboratory, Immunosciences Lab., Inc., in the past four years. Our leading investigative efforts have been followed by many other researchers which has resulted in the detection of heightened levels of antibodies against more than 20 tissue antigens in individuals infected with SARS-CoV-2.
This is why measurement of antibodies against SARS-CoV-2, EBV, HHV-6/7 and their component proteins and antigens are crucial in the effective prediction, prevention and management of not just long COVID and its overlap with ME/CFS but autoimmune diseases as well.
Vojdani A, Vojdani E, Saidara E, Maes M. Persistent SARS-CoV-2 Infection, EBV, HHV-6 and other factors may contribute to inflammation and autoimmunity in long COVID. Viruses, 15(2):400, 2023, doi: 10.3390/v15020400.
Vojdani, A., Almulla A. F., Bo Z., Hussein K. A.-H. and Maes M. Reactivation of herpesvirus type-6 and IgA/IgM-mediated responses to activin-A underpin Long COVID, including affective symptoms and chronic fatigue syndrome. Acta Neuropsychiatrica, 2024, 4:1-13, doi: 10.1017/neu.2024.10.
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