key: cord-0745953-2e8zj1we
authors: Drosos, Alexandros A.; Pelechas, Eleftherios; Voulgari, Paraskevi V.
title: Long COVID from rheumatology perspective: a simple mimicker or promoter of autoimmunity?
date: 2022-02-11
journal: Clin Rheumatol
DOI: 10.1007/s10067-022-06092-4
sha: a4da8c31b4d14372f5ba0112f6c8a7f789ca3e6f
doc_id: 745953
cord_uid: 2e8zj1we

nan

We have read with great interest the review article by Sapkota et al. which has been recently published in the Clinical Rheumatology journal dealing with long COVID [1] . In this paper, the authors reported the symptoms and immunological findings of patients who were infected from severe acute respiratory syndrome coronovirus-2 (SARS-CoV-2). These symptoms and laboratory features share similarities with those of patients suffering from autoimmune rheumatic diseases (ARDs). They concluded that long COVID is a mimicker of ARDs and needs to be excluded to ensure a correct diagnosis [1] .

Recently, we reported a patient who contracted SARS-CoV-2 infection and developed an erosive seronegative arthritis six months after infection [2] . Musculoskeletal, cutaneous, and other systemic manifestations, along with the presence of autoantibodies, are frequently observed in these patients. On the other hand, SARS-CoV-2 may trigger autoimmune responses and the development of denovo manifestations of ARDs, as in our patient [3] . The pathogenesis of these phenomena is not well defined. One hypothesis implies the presence of autoantibodies against interferon (IFN) type-I, or inborn errors in the type-I IFN immunity [4, 5] . Another hypothesis is that SARS-CoV-2 might trigger autoimmune responses through molecular mimicry [3] . Several viruses have been implicated as possible etiological factors for the development of ARDs, mostly systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and others. Between viruses Epstein-Barr virus (EBV) is implicated in the pathogenesis of the above disorders [3, 6] . Indeed, EBV can trigger immune responses through molecular mimicry and is a polyclonal activator of B-cells and increases the production of rheumatoid factor (RF). Several studies suggested that molecular mimicry is a possible mechanism responsible for the development of ARDs in SARS-CoV-2 infection [7, 8] . Thus, SARS-CoV-2 may trigger autoimmunity and the possible development of the de novo manifestations of ARDs.

Disclosures None.

Long COVID from rheumatology perspective -a narrative review

Seronegative Erosive Arthritis Following SARS-CoV-2 Infection

Systemic and organ-specific immune-related manifestations of COVID-19

Autoantibodies against type I IFNs in patients with life-threatening COVID-19

Inborn errors of type I IFN immunity in patients with life-threatening COVID-19

Association of Epstein-Barr virus serological reactivation with transitioning to This comment refers to the article available online at

systemic lupus erythematosus in at risk-individuals

Human molecular chaperons share with SARS-CoV-2 antigenic epitopes potentially capable of eliciting autoimmunity against endothelial cells: possible role of molecular mimicry in COVID-19

Molecular mimicry between SARS-CoV-2 and respiratory pacemaker neurons

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